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Large-scale efforts have been persistently undertaken for medical prophylaxis and treatment of COVID-19 disasters worldwide. A variety of novel viral spike protein-targeted vaccines have been extensively distributed for global inoculation based on accelerated approval. With concerns of emerging spike protein mutations, we revisited the early but inconclusive clinical interest in the repurposed combination of azithromycin (AZT) and zinc supplements with safety advantages. The aim of this study is to provide in vitro proof of concept for IκBα associated rapid and synergistic suppression of angiotensin-converting enzymes 2 (ACE2) following combination treatments with AZT plus zinc sulfate in two human airway cells with ACE2 expression, Calu-3 and H322M, representative cells of the human upper and lower airway origin respectively. Clinical timing of AZT combined with zinc is indicated based on suppression of the key cellular entry molecule, ACE2, of SARS-CoV-2.
Chia-Wei Chang; Ming-Cheng Lee; Bor-Ru Lin; Yen-Pei Lu; Yih-Jen Hsu; Chun-Yu Chuang; Tsung-Tao Huang; Yin-Kai Chen. The Effect of Azithromycin Plus Zinc Sulfate on ACE2 Expression through IκBα of Human Respiratory Cells in SARS-CoV-2: In Vitro Study. COVID 2021, 1, 263 -275.
AMA StyleChia-Wei Chang, Ming-Cheng Lee, Bor-Ru Lin, Yen-Pei Lu, Yih-Jen Hsu, Chun-Yu Chuang, Tsung-Tao Huang, Yin-Kai Chen. The Effect of Azithromycin Plus Zinc Sulfate on ACE2 Expression through IκBα of Human Respiratory Cells in SARS-CoV-2: In Vitro Study. COVID. 2021; 1 (1):263-275.
Chicago/Turabian StyleChia-Wei Chang; Ming-Cheng Lee; Bor-Ru Lin; Yen-Pei Lu; Yih-Jen Hsu; Chun-Yu Chuang; Tsung-Tao Huang; Yin-Kai Chen. 2021. "The Effect of Azithromycin Plus Zinc Sulfate on ACE2 Expression through IκBα of Human Respiratory Cells in SARS-CoV-2: In Vitro Study." COVID 1, no. 1: 263-275.
Angiotensin-converting enzyme 2 (ACE2) is a key negative regulator of the renin-angiotensin system and also a major receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Here, we reveal a role for NF-κB in human lung cell expression of ACE2, and we further explore the potential utility of repurposing NF-κB inhibitors to downregulate ACE2. Expression of ACE2 was assessed by Western blotting and RT-qPCR in multiple human lung cell lines with or without NF-κB inhibitor treatment. Surface ACE2 expression and intracellular reactive oxygen species (ROS) levels were measured with flow cytometry. p50 was knocked down with siRNA. Cytotoxicity was monitored by PARP cleavage and MTS assay. Pyrrolidine dithiocarbamate (PDTC), an NF-κB inhibitor, suppressed endogenous ACE2 mRNA and protein expression in H322M and Calu-3 cells. The ROS level in H322M cells was increased after PDTC treatment, and pretreatment with N-acetyl-cysteine (NAC) reversed PDTC-induced ACE2 suppression. Meanwhile, treatment with hydrogen peroxide augmented ACE2 suppression in H322M cells with p50 knockdown. Two repurposed NF-κB inhibitors, the anthelmintic drug triclabendazole and the antiprotozoal drug emetine, also reduced ACE2 mRNA and protein levels. Moreover, zinc supplementation augmented the suppressive effects of triclabendazole and emetine on ACE2 expression in H322M and Calu-3 cells. These results suggest that ACE2 expression is modulated by ROS and NF-κB signaling in human lung cells, and the combination of zinc with triclabendazole or emetine shows promise for clinical treatment of ACE2-related disease.
Ming-Cheng Lee; Yin-Kai Chen; Jyy-Jih Tsai-Wu; Yih-Jen Hsu; Bor-Ru Lin. Zinc supplementation augments the suppressive effects of repurposed NF-κB inhibitors on ACE2 expression in human lung cell lines. Life Sciences 2021, 280, 119752 -119752.
AMA StyleMing-Cheng Lee, Yin-Kai Chen, Jyy-Jih Tsai-Wu, Yih-Jen Hsu, Bor-Ru Lin. Zinc supplementation augments the suppressive effects of repurposed NF-κB inhibitors on ACE2 expression in human lung cell lines. Life Sciences. 2021; 280 ():119752-119752.
Chicago/Turabian StyleMing-Cheng Lee; Yin-Kai Chen; Jyy-Jih Tsai-Wu; Yih-Jen Hsu; Bor-Ru Lin. 2021. "Zinc supplementation augments the suppressive effects of repurposed NF-κB inhibitors on ACE2 expression in human lung cell lines." Life Sciences 280, no. : 119752-119752.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes a vast number of infections and fatalities worldwide. As the development and safety validation of effective vaccines are ongoing, drug repurposing is most efficient approach to search FDA approved agents against coronavirus disease 2019 (COVID-19). In the present study, we found that endogenous ACE2 expressions could be detected in H322M and Calu-3 cell lines, as well as their ACE2 mRNA and protein expressions were suppressed by pyrrolidine dithiocarbamate (PDTC), a NF-kappa B inhibitor, in dose- and time-dependent manners. Moreover, N-acetyl-cysteine (NAC) pretreatment reversed PDTC-induced ACE2 suppression, as well as the combined treatment of hydrogen peroxide and knockdown of p50 subunit of NF-kappa B by siRNA reduced ACE2 expression in H322M cells. In addition, anthelmintic drug triclabendazole and antiprotozoal drug emetine, repurposed drugs of NF-kappa B inhibitor, also inhibited ACE2 mRNA and protein expressions in H322M cells. Moreover, zinc supplement augmented the suppressive effects of triclabendazole and emetine on ACE2 suppression in H322M and Calu-3 cells. Taken together, these results indicate that ACE2 expression is modulated by reactive oxygen species (ROS) and NF-kappa B signal in human lung cell lines, and zinc combination with triclabendazole or emetine has the clinical potential for the prevention and treatment of COVID-19.
Ming-Cheng Lee; Yin-Kai Chen; Yih-Jen Hsu; Bor-Ru Lin. Zinc supplement augments the suppressive effects of repurposed drugs of NF-kappa B inhibitor on ACE2 expression in human lung cell lines in vitro. 2021, 1 .
AMA StyleMing-Cheng Lee, Yin-Kai Chen, Yih-Jen Hsu, Bor-Ru Lin. Zinc supplement augments the suppressive effects of repurposed drugs of NF-kappa B inhibitor on ACE2 expression in human lung cell lines in vitro. . 2021; ():1.
Chicago/Turabian StyleMing-Cheng Lee; Yin-Kai Chen; Yih-Jen Hsu; Bor-Ru Lin. 2021. "Zinc supplement augments the suppressive effects of repurposed drugs of NF-kappa B inhibitor on ACE2 expression in human lung cell lines in vitro." , no. : 1.
Chi-Tan Hu; Chien-Chih Tung; Chun-Jung Lin; I-Nan Kuo; Bor-Ru Lin; Hong-Long Wang; Jin-De Chen; Mu-Liang Cheng; Chia-Tung Shun; Hui-Mi Li; Jui-Sheng Hung; Wei-Yi Lei; Ming Jium Shieh; Jau-Min Wong; John Y. Kao; Jyh-Chin Yang. 52 - Efficacy of High-Dose Dual Therapy Versus Bismuth Quadruple Therapy for Rescue Treatment of Helicobacter Pylori — An Interim Report of Multi-Center, Randomized Control Study. Gastroenterology 2018, 154, 1 -18.
AMA StyleChi-Tan Hu, Chien-Chih Tung, Chun-Jung Lin, I-Nan Kuo, Bor-Ru Lin, Hong-Long Wang, Jin-De Chen, Mu-Liang Cheng, Chia-Tung Shun, Hui-Mi Li, Jui-Sheng Hung, Wei-Yi Lei, Ming Jium Shieh, Jau-Min Wong, John Y. Kao, Jyh-Chin Yang. 52 - Efficacy of High-Dose Dual Therapy Versus Bismuth Quadruple Therapy for Rescue Treatment of Helicobacter Pylori — An Interim Report of Multi-Center, Randomized Control Study. Gastroenterology. 2018; 154 (6):1-18.
Chicago/Turabian StyleChi-Tan Hu; Chien-Chih Tung; Chun-Jung Lin; I-Nan Kuo; Bor-Ru Lin; Hong-Long Wang; Jin-De Chen; Mu-Liang Cheng; Chia-Tung Shun; Hui-Mi Li; Jui-Sheng Hung; Wei-Yi Lei; Ming Jium Shieh; Jau-Min Wong; John Y. Kao; Jyh-Chin Yang. 2018. "52 - Efficacy of High-Dose Dual Therapy Versus Bismuth Quadruple Therapy for Rescue Treatment of Helicobacter Pylori — An Interim Report of Multi-Center, Randomized Control Study." Gastroenterology 154, no. 6: 1-18.
Chi-Tan Hu; Chien-Chih Tung; Chun-Jung Lin; I-Nan Kuo; Bor-Ru Lin; Hong-Long Wang; Jin-De Chen; Mu-Liang Cheng; Chia-Tung Shun; Huei-Mi Li; Jui-Sheng Hung; Wei-Yi Lei; Ming Jium Shieh; Jau-Min Wong; John Y. Kao; Jyh-Chin Yang. Efficacy of High-Dose Dual Therapy Versus Bismuthcontaining Quadruple Therapy for First-Line Treatment of Helicobacter Pylori Infection and an Interim Report of Multi-Center, Randomized Control Study. Gastroenterology 2017, 152, S182 -S183.
AMA StyleChi-Tan Hu, Chien-Chih Tung, Chun-Jung Lin, I-Nan Kuo, Bor-Ru Lin, Hong-Long Wang, Jin-De Chen, Mu-Liang Cheng, Chia-Tung Shun, Huei-Mi Li, Jui-Sheng Hung, Wei-Yi Lei, Ming Jium Shieh, Jau-Min Wong, John Y. Kao, Jyh-Chin Yang. Efficacy of High-Dose Dual Therapy Versus Bismuthcontaining Quadruple Therapy for First-Line Treatment of Helicobacter Pylori Infection and an Interim Report of Multi-Center, Randomized Control Study. Gastroenterology. 2017; 152 (5):S182-S183.
Chicago/Turabian StyleChi-Tan Hu; Chien-Chih Tung; Chun-Jung Lin; I-Nan Kuo; Bor-Ru Lin; Hong-Long Wang; Jin-De Chen; Mu-Liang Cheng; Chia-Tung Shun; Huei-Mi Li; Jui-Sheng Hung; Wei-Yi Lei; Ming Jium Shieh; Jau-Min Wong; John Y. Kao; Jyh-Chin Yang. 2017. "Efficacy of High-Dose Dual Therapy Versus Bismuthcontaining Quadruple Therapy for First-Line Treatment of Helicobacter Pylori Infection and an Interim Report of Multi-Center, Randomized Control Study." Gastroenterology 152, no. 5: S182-S183.
Jyh-Chin Yang; Chun-Jung Lin; Huei-Mi Li; Chien-Chih Tung; John Y. Kao; Jin-De Chen; Bor-Ru Lin; Ming Jium Shieh; Ming-Chu Chang; Yu-Ting Chang; Shu-Chen Wei; Jau-Min Wong. 316 Genotypic Testing Is Suboptimal to Predict Antibiotic Resistance and Therapeutic Outcome for Helicobacter pylori Eradication in Clinical Practice. Gastroenterology 2016, 150, S73 .
AMA StyleJyh-Chin Yang, Chun-Jung Lin, Huei-Mi Li, Chien-Chih Tung, John Y. Kao, Jin-De Chen, Bor-Ru Lin, Ming Jium Shieh, Ming-Chu Chang, Yu-Ting Chang, Shu-Chen Wei, Jau-Min Wong. 316 Genotypic Testing Is Suboptimal to Predict Antibiotic Resistance and Therapeutic Outcome for Helicobacter pylori Eradication in Clinical Practice. Gastroenterology. 2016; 150 (4):S73.
Chicago/Turabian StyleJyh-Chin Yang; Chun-Jung Lin; Huei-Mi Li; Chien-Chih Tung; John Y. Kao; Jin-De Chen; Bor-Ru Lin; Ming Jium Shieh; Ming-Chu Chang; Yu-Ting Chang; Shu-Chen Wei; Jau-Min Wong. 2016. "316 Genotypic Testing Is Suboptimal to Predict Antibiotic Resistance and Therapeutic Outcome for Helicobacter pylori Eradication in Clinical Practice." Gastroenterology 150, no. 4: S73.
Jyh-Chin Yang; Chun-Jung Lin; Jin-De Chen; Hong-Long Wang; John Y. Kao; Bor-Ru Lin; Ming Jium Shieh; Ming-Chu Chang; Yu-Ting Chang; Shu-Chen Wei; Chien-Chih Tung; Jau-Min Wong. 770 High Cumulative Eradication Rate in the First-Line and Rescue Therapies for Helicobacter pylori Infection by Repeated Optimized High Dose Dual Therapy. Gastroenterology 2015, 148, 1 -149.
AMA StyleJyh-Chin Yang, Chun-Jung Lin, Jin-De Chen, Hong-Long Wang, John Y. Kao, Bor-Ru Lin, Ming Jium Shieh, Ming-Chu Chang, Yu-Ting Chang, Shu-Chen Wei, Chien-Chih Tung, Jau-Min Wong. 770 High Cumulative Eradication Rate in the First-Line and Rescue Therapies for Helicobacter pylori Infection by Repeated Optimized High Dose Dual Therapy. Gastroenterology. 2015; 148 (4):1-149.
Chicago/Turabian StyleJyh-Chin Yang; Chun-Jung Lin; Jin-De Chen; Hong-Long Wang; John Y. Kao; Bor-Ru Lin; Ming Jium Shieh; Ming-Chu Chang; Yu-Ting Chang; Shu-Chen Wei; Chien-Chih Tung; Jau-Min Wong. 2015. "770 High Cumulative Eradication Rate in the First-Line and Rescue Therapies for Helicobacter pylori Infection by Repeated Optimized High Dose Dual Therapy." Gastroenterology 148, no. 4: 1-149.
Cresols are present in antiseptics, coal tar, some resins, pesticides, and industrial solvents. Cresol intoxication leads to hepatic injury due to coagulopathy as well as disturbance of hepatic circulation in fatal cases. Patients with uremia suffer from cardiovascular complications, such as atherosclerosis, thrombosis, hemolysis, and bleeding, which may be partly due to p-cresol toxicity and its effects on vascular endothelial and mononuclear cells. Given the role of reactive oxygen species (ROS) and inflammation in vascular thrombosis, the objective of this study was to evaluate the effect of p-cresol on endothelial and mononuclear cells. EA.hy926 (EAHY) endothelial cells and U937 cells were exposed to different concentrations of p-cresol. Cytotoxicity was evaluated by 3-(4,5-Dimethylthiazol-2-yl)-2,5 -diphenyltetrazolium bromide (MTT) assay and trypan blue dye exclusion technique, respectively. Cell cycle distribution was analyzed by propidium iodide flow cytometry. Endothelial cell migration was studied by wound closure assay. ROS level was measured by 2′,7′-dichlorofluorescein diacetate (DCF) fluorescence flow cytometry. Prostaglandin F2α (PGF2α), plasminogen activator inhibitor-1 (PAI-1), soluble urokinase plasminogen activator receptor (suPAR), and uPA production were determined by Enzyme-linked immunosorbant assay (ELISA). Exposure to 100–500 µM p-cresol decreased EAHY cell number by 30–61%. P-cresol also decreased the viability of U937 mononuclear cells. The inhibition of EAHY and U937 cell growth by p-cresol was related to induction of S-phase cell cycle arrest. Closure of endothelial wounds was inhibited by p-cresol (>100 µM). P-cresol (>50 µM) also stimulated ROS production in U937 cells and EAHY cells but to a lesser extent. Moreover, p-cresol markedly stimulated PAI-1 and suPAR, but not PGF2α, and uPA production in EAHY cells. p-Cresol may contribute to atherosclerosis and thrombosis in patients with uremia and cresol intoxication possibly due to induction of ROS, endothelial/mononuclear cell damage and production of inflammation/atherosclerosis-related molecules.
Mei-Chi Chang; Hsiao-Hua Chang; Chiu-Po Chan; Sin-Yuet Yeung; Hsiang-Chi Hsien; Bor-Ru Lin; Chien-Yang Yeh; Wan-Yu Tseng; Shui-Kuan Tseng; Jiiang-Huei Jeng. p-Cresol Affects Reactive Oxygen Species Generation, Cell Cycle Arrest, Cytotoxicity and Inflammation/Atherosclerosis-Related Modulators Production in Endothelial Cells and Mononuclear Cells. PLOS ONE 2014, 9, e114446 .
AMA StyleMei-Chi Chang, Hsiao-Hua Chang, Chiu-Po Chan, Sin-Yuet Yeung, Hsiang-Chi Hsien, Bor-Ru Lin, Chien-Yang Yeh, Wan-Yu Tseng, Shui-Kuan Tseng, Jiiang-Huei Jeng. p-Cresol Affects Reactive Oxygen Species Generation, Cell Cycle Arrest, Cytotoxicity and Inflammation/Atherosclerosis-Related Modulators Production in Endothelial Cells and Mononuclear Cells. PLOS ONE. 2014; 9 (12):e114446.
Chicago/Turabian StyleMei-Chi Chang; Hsiao-Hua Chang; Chiu-Po Chan; Sin-Yuet Yeung; Hsiang-Chi Hsien; Bor-Ru Lin; Chien-Yang Yeh; Wan-Yu Tseng; Shui-Kuan Tseng; Jiiang-Huei Jeng. 2014. "p-Cresol Affects Reactive Oxygen Species Generation, Cell Cycle Arrest, Cytotoxicity and Inflammation/Atherosclerosis-Related Modulators Production in Endothelial Cells and Mononuclear Cells." PLOS ONE 9, no. 12: e114446.
Background & Aims The efficacy of treatment of Helicobacter pylori infection has decreased steadily because of increasing resistance to clarithromycin, metronidazole, and levofloxacin. Resistance to amoxicillin is generally low, and high intragastric pH increases the efficacy of amoxicillin, so we investigated whether a combination of a high-dose proton pump inhibitor and amoxicillin (dual therapy) was more effective than standard first-line or rescue therapies in eradicating H pylori. Methods We performed a large-scale multihospital trial to compare the efficacy of a high-dose dual therapy (HDDT) with that of standard therapies in treatment-naive (n = 450) or treatment-experienced (n = 168) patients with H pylori infection. Treatment-naive patients were randomly assigned to groups given HDDT (rabeprazole 20 mg and amoxicillin 750 mg, 4 times/day for 14 days, group A1), sequential therapy for 10 days (group B1), or clarithromycin-containing triple therapy for 7 days (group C1). Treatment-experienced patients were randomly assigned to groups given HDDT for 14 days (group A2), sequential therapy for 10 days (B2), or levofloxacin-containing triple therapy for 7 days (C2). H pylori infection was detected by using the 13C-urea breath test. We evaluated factors associated with treatment outcomes. Results In the intention-to-treat analysis, H pylori was eradicated in 95.3% of patients in group A1 (95% confidence interval [CI], 91.9%−98.8%), 85.3% in B1 (95% CI, 79.6%−91.1%), and 80.7% in group C1 (95% CI, 74.3%−87.1%). Infection was eradicated in 89.3% of patients in group A2 (95% CI, 80.9%−97.6%), 51.8% in group B2 (95% CI, 38.3%−65.3%), and 78.6% (95% CI, 67.5%−89.7%) in group C2. The efficacy of HDDT was significantly higher than that of currently recommended regimens, irrespective of CYP2C19 genotype. Bacterial resistance to drugs was associated with treatment failure. There were no significant differences between groups in adverse events or patient adherence. Conclusions HDDT is superior to standard regimens as empirical first-line or rescue therapy for H pylori infection, with similar safety profiles and tolerability. ClinicalTrials.gov number: NCT01163435.
Jyh-Chin Yang; Chun-Jung Lin; Hong-Long Wang; Jin-De Chen; John Y. Kao; Chia-Tung Shun; Chien-Wei Lu; Bor-Ru Lin; Ming-Jium Shieh; Ming-Chu Chang; Yu-Ting Chang; Shu-Chen Wei; Lin-Chih Lin; Wen-Chun Yeh; Jen-Shin Kuo; Chien-Chih Tung; Yew-Loong Leong; Teh-Hong Wang; Jau-Min Wong. High-dose Dual Therapy Is Superior to Standard First-line or Rescue Therapy for Helicobacter pylori Infection. Clinical Gastroenterology and Hepatology 2014, 13, 895 -905.e5.
AMA StyleJyh-Chin Yang, Chun-Jung Lin, Hong-Long Wang, Jin-De Chen, John Y. Kao, Chia-Tung Shun, Chien-Wei Lu, Bor-Ru Lin, Ming-Jium Shieh, Ming-Chu Chang, Yu-Ting Chang, Shu-Chen Wei, Lin-Chih Lin, Wen-Chun Yeh, Jen-Shin Kuo, Chien-Chih Tung, Yew-Loong Leong, Teh-Hong Wang, Jau-Min Wong. High-dose Dual Therapy Is Superior to Standard First-line or Rescue Therapy for Helicobacter pylori Infection. Clinical Gastroenterology and Hepatology. 2014; 13 (5):895-905.e5.
Chicago/Turabian StyleJyh-Chin Yang; Chun-Jung Lin; Hong-Long Wang; Jin-De Chen; John Y. Kao; Chia-Tung Shun; Chien-Wei Lu; Bor-Ru Lin; Ming-Jium Shieh; Ming-Chu Chang; Yu-Ting Chang; Shu-Chen Wei; Lin-Chih Lin; Wen-Chun Yeh; Jen-Shin Kuo; Chien-Chih Tung; Yew-Loong Leong; Teh-Hong Wang; Jau-Min Wong. 2014. "High-dose Dual Therapy Is Superior to Standard First-line or Rescue Therapy for Helicobacter pylori Infection." Clinical Gastroenterology and Hepatology 13, no. 5: 895-905.e5.
Gastroesophageal flap valve (GEFV) endoscopic grading is reported to be associated with gastroesophageal reflux disease (GERD) in adults; however its role in pediatric groups remains unknown. This study aimed to investigate the significance of GEFV grading and the associations to multichannel intraluminal impedance and pH monitoring (MII-pH) in children with GERD. A total of 48 children with GERD symptoms who received esophagogastroduodenoscopy and MII-pH monitoring were enrolled. The degree of GEFV was graded from I to IV according to the Hill classification, and classified into two groups: normal GEFV (Hill grades I and II), and abnormal GEFV (Hill grades III and VI). Endoscopic findings and MII-pH monitoring were analyzed among the groups. Thirty-six patients had normal GEFV while 12 had abnormal GEFV. The presence of erosive esophagitis was significantly more common in the patients with abnormal GEFV (p = 0.037, OR 9.84, 95% CI 1.15–84.42). Pathological acidic gastroesophageal reflux (GER) determined by MII-pH was more prevalent in the patients with loosened GEFV geometry (p = 0.01, OR 7.0, 95% CI 1.67–27.38). There were significant positive correlations between GEFV Hill grading I to IV and the severity of erosive esophagitis (r = 0.49, p<0.001), percentage of supine acid reflux (r = 0.37, p = 0.009), percentage of total acid reflux (r = 0.3284, p = 0.023), and DeMeester score (r = 0.36, p = 0.01) detected by pH monitoring. In the impedance study, GEFV Hill grading also positively correlated to median number of acid reflux events (r = 0.3015, p = 0.037). GEFV dysfunction highly associated with acid GER and severe erosive esophagitis. An abnormal GEFV is a sign of acid GER in children.
Kai-Chi Chang; Jia-Feng Wu; Wei-Chung Hsu; Bor-Ru Lin; Huey-Ling Chen; Yen-Hsuan Ni. Impacts of Endoscopic Gastroesophageal Flap Valve Grading on Pediatric Gastroesophageal Reflux Disease. PLOS ONE 2014, 9, e107954 .
AMA StyleKai-Chi Chang, Jia-Feng Wu, Wei-Chung Hsu, Bor-Ru Lin, Huey-Ling Chen, Yen-Hsuan Ni. Impacts of Endoscopic Gastroesophageal Flap Valve Grading on Pediatric Gastroesophageal Reflux Disease. PLOS ONE. 2014; 9 (9):e107954.
Chicago/Turabian StyleKai-Chi Chang; Jia-Feng Wu; Wei-Chung Hsu; Bor-Ru Lin; Huey-Ling Chen; Yen-Hsuan Ni. 2014. "Impacts of Endoscopic Gastroesophageal Flap Valve Grading on Pediatric Gastroesophageal Reflux Disease." PLOS ONE 9, no. 9: e107954.
Catechol (benzenediol) is present in plant-derived products, such as vegetables, fruits, coffee, tea, wine, areca nut and cigarette smoke. Because platelet dysfunction is a risk factor of cardiovascular diseases, including stroke, atherosclerosis and myocardial infarction, the purpose of this study was to evaluate the anti-platelet and anti-inflammatory effect of catechol and its mechanisms. The effects of catechol on cyclooxygenase (COX) activity, arachidonic acid (AA)-induced aggregation, thromboxane B2 (TXB2) production, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) production and extracellular signal-regulated kinase (ERK)/p38 phosphorylation were determined in rabbit platelets. In addition, its effect on IL-1β-induced prostaglandin E2 (PGE2) production by fibroblasts was determined. The ex vivo effect of catechol on platelet aggregation was also measured. Catechol (5-25 µM) suppressed AA-induced platelet aggregation and inhibited TXB2 production at concentrations of 0.5–5 µM; however, it showed little cytotoxicity and did not alter U46619-induced platelet aggregation. Catechol (10–50 µM) suppressed COX-1 activity by 29–44% and COX-2 activity by 29–50%. It also inhibited IL-1β-induced PGE2 production, but not COX-2 expression of fibroblasts. Moreover, catechol (1–10 µM) attenuated AA-induced ROS production in platelets and phorbol myristate acetate (PMA)-induced ROS production in human polymorphonuclear leukocytes. Exposure of platelets to catechol decreased AA-induced ERK and p38 phosphorylation. Finally, intravenous administration of catechol (2.5–5 µmole/mouse) attenuated ex vivo AA-induced platelet aggregation. These results suggest that catechol exhibited anti-platelet and anti-inflammatory effects, which were mediated by inhibition of COX, ROS and TXA2 production as well as ERK/p38 phosphorylation. The anti-platelet effect of catechol was confirmed by ex vivo analysis. Exposure to catechol may affect platelet function and thus cardiovascular health.
Mei-Chi Chang; Hsiao-Hua Chang; Tong-Mei Wang; Chiu-Po Chan; Bor-Ru Lin; Sin-Yuet Yeung; Chien-Yang Yeh; Ru-Hsiu Cheng; Jiiang-Huei Jeng. Antiplatelet Effect of Catechol Is Related to Inhibition of Cyclooxygenase, Reactive Oxygen Species, ERK/p38 Signaling and Thromboxane A2 Production. PLOS ONE 2014, 9, e104310 .
AMA StyleMei-Chi Chang, Hsiao-Hua Chang, Tong-Mei Wang, Chiu-Po Chan, Bor-Ru Lin, Sin-Yuet Yeung, Chien-Yang Yeh, Ru-Hsiu Cheng, Jiiang-Huei Jeng. Antiplatelet Effect of Catechol Is Related to Inhibition of Cyclooxygenase, Reactive Oxygen Species, ERK/p38 Signaling and Thromboxane A2 Production. PLOS ONE. 2014; 9 (8):e104310.
Chicago/Turabian StyleMei-Chi Chang; Hsiao-Hua Chang; Tong-Mei Wang; Chiu-Po Chan; Bor-Ru Lin; Sin-Yuet Yeung; Chien-Yang Yeh; Ru-Hsiu Cheng; Jiiang-Huei Jeng. 2014. "Antiplatelet Effect of Catechol Is Related to Inhibition of Cyclooxygenase, Reactive Oxygen Species, ERK/p38 Signaling and Thromboxane A2 Production." PLOS ONE 9, no. 8: e104310.
One newly bred variety of tea cultivar, purple-shoot tea, was selected to evaluate its antiproliferative effects on colorectal carcinoma cells, as well as normal colon cells. The phytochemicals and identified catechins of purple-shoot tea extract (PTE) were significantly higher than that of ordinary tea, especially the anthocyanins (surpassed by 135-fold) and anthocyanidins (surpassed by 3.5-fold). PTE inhibited the proliferation of COLO 320DM (IC50 = 64.9 μg/mL) and HT-29 (IC50 = 55.2 μg/mL) by blocking cell cycle progression during the G0/G1 phase and inducing apoptotic death. Western blotting indicated that PTE induced cell cycle arrest by reducing the expression of cyclin E and cyclin D1 in COLO 320DM and the upregulation of p21 and p27 cyclin-dependent kinase inhibitors in HT-29. Two cells treated with PTE also indicated the cleavage of PARP, activation of caspase 3, and an increased Bax/Bcl-2 ratio. Our results showed that PTE is a potential novel dietary agent for colorectal cancer chemoprevention.
Chih-Ping Hsu; Yi-Ting Shih; Bor-Ru Lin; Chui-Feng Chiu; Chih-Cheng Lin. Inhibitory Effect and Mechanisms of an Anthocyanins- and Anthocyanidins-Rich Extract from Purple-Shoot Tea on Colorectal Carcinoma Cell Proliferation. Journal of Agricultural and Food Chemistry 2012, 60, 3686 -3692.
AMA StyleChih-Ping Hsu, Yi-Ting Shih, Bor-Ru Lin, Chui-Feng Chiu, Chih-Cheng Lin. Inhibitory Effect and Mechanisms of an Anthocyanins- and Anthocyanidins-Rich Extract from Purple-Shoot Tea on Colorectal Carcinoma Cell Proliferation. Journal of Agricultural and Food Chemistry. 2012; 60 (14):3686-3692.
Chicago/Turabian StyleChih-Ping Hsu; Yi-Ting Shih; Bor-Ru Lin; Chui-Feng Chiu; Chih-Cheng Lin. 2012. "Inhibitory Effect and Mechanisms of an Anthocyanins- and Anthocyanidins-Rich Extract from Purple-Shoot Tea on Colorectal Carcinoma Cell Proliferation." Journal of Agricultural and Food Chemistry 60, no. 14: 3686-3692.
P-cresol is a well-known uremic toxin and environmental toxicant that may affect platelet functions. In this study, p-cresol (1-5 μM) inhibited the arachidonic acid (AA)-induced platelet aggregation, with 47% and 82% of inhibition at concentrations of 2 and 5 μM, respectively. Under similar experimental condition, p-cresol showed little effect on the U46619-induced platelet aggregation. p-cresol (<500 μM) revealed no discernable cytotoxicity to platelets as analyzed by quantification of lactate dehydrogenase release. Antiplatelet effect of p-cresol was related to inhibition of thromboxane A(2) (TXA(2)) and prostaglandin D(2) (PGD(2)) formation. P-cresol (2-100 μM) partly inhibited the AA-induced reactive oxygen species (ROS) production as well as the extracellular signal-regulated kinase (ERK1/2) and p38 phosphorylation in platelets. P-cresol further inhibited the AA-induced aggregation of rabbit platelet-rich plasma (PRP) with an IC50 of 2 μM and aggregation of human PRP (IC50 = 13.6 μM). Intravenous administration of p-cresol (250-1000 nmole) into mice effectively suppressed the ex vivo platelet aggregation, whereas showed little effect on the value of RBC, hemoglobin (HGB), hematocrit, MCV, MCH, MCHC, platelets and lymphocyte counts. These results indicate that in acute p-cresol-poisoning and long-term exposure to cresol as in severe uremic patients, p-cresol may potentially inhibit blood clot formation and lead to hemorrhagic disorders via inhibition of platelet aggregation, ROS production, ERK/p38 activation and TXA(2) production.
Mei-Chi Chang; Tong-Mei Wang; Sin-Yuet Yeung; Po-Yuan Jeng; Hsiang-Ruei Liao; Tzu-Yung Lin; Chiu-Chun Lin; Bor-Ru Lin; Jiiang-Huei Jeng. Antiplatelet effect by p-cresol, a uremic and environmental toxicant, is related to inhibition of reactive oxygen species, ERK/p38 signaling and thromboxane A2 production. Atherosclerosis 2011, 219, 559 -565.
AMA StyleMei-Chi Chang, Tong-Mei Wang, Sin-Yuet Yeung, Po-Yuan Jeng, Hsiang-Ruei Liao, Tzu-Yung Lin, Chiu-Chun Lin, Bor-Ru Lin, Jiiang-Huei Jeng. Antiplatelet effect by p-cresol, a uremic and environmental toxicant, is related to inhibition of reactive oxygen species, ERK/p38 signaling and thromboxane A2 production. Atherosclerosis. 2011; 219 (2):559-565.
Chicago/Turabian StyleMei-Chi Chang; Tong-Mei Wang; Sin-Yuet Yeung; Po-Yuan Jeng; Hsiang-Ruei Liao; Tzu-Yung Lin; Chiu-Chun Lin; Bor-Ru Lin; Jiiang-Huei Jeng. 2011. "Antiplatelet effect by p-cresol, a uremic and environmental toxicant, is related to inhibition of reactive oxygen species, ERK/p38 signaling and thromboxane A2 production." Atherosclerosis 219, no. 2: 559-565.
Gut barrier dysfunction and bacterial translocation occur in various disorders, including intestinal obstruction. Overexpression of inducible nitric oxide synthase is implicated in the pathogenesis of bacterial translocation, of which the molecular mechanism remains unclear. Epithelial permeability is regulated by tight junction reorganization and myosin light chain phosphorylation. Our aim was to investigate the roles of Rho-associated kinase and protein kinase C ζ in epithelial nitric oxide synthase-mediated barrier damage. Animal study and cell cultures. Research laboratory. BALB/c mice. Mouse distal small intestine was obstructed in vivo by a 10-cm loop ligation in which vehicle, L-Nil (a nitric oxide synthase inhibitor), or Y27632 (a Rho-associated kinase inhibitor) was luminally administered. After obstruction for 24 hrs, intestinal tissues were mounted on Ussing chambers for macromolecular flux. Liver and spleen tissues were assessed for bacterial counts. Caco-2 cells were exposed to 1 mM S-nitroso-N-acetylpenicillamine (a nitric oxide donor) for 24 hrs, and transepithelial resistance and permeability were evaluated. Mice with intestinal obstruction displayed epithelial barrier dysfunctions, such as permeability rise and bacterial translocation, associated with tight junction disruption and myosin light chain phosphorylation. Increased inducible nitric oxide synthase and phosphorylated protein kinase C ζ were observed in villus epithelium. Enteric instillation of L-Nil and Y27632 attenuated the functional and structural barrier damage caused by intestinal obstruction. L-Nil decreased intestinal obstruction-induced myosin light chain, myosin phosphatase target subunit 1, and protein kinase C ζ phosphorylation, suggesting that inducible nitric oxide synthase is upstream of Rho-associated kinase and protein kinase C ζ signaling. The intestinal phosphorylated myosin light chain level did not increase in inducible nitric oxide synthase(−/−) mice following intestinal obstruction. In vitro studies showed that S-nitroso-N-acetylpenicillamine-induced transepithelial resistance drop and permeability rise was independent of cell apoptosis. Y27632 inhibited S-nitroso-N-acetylpenicillamine-induced myosin light chain phosphorylation and permeability rise. S-nitroso-N-acetylpenicillamine also triggered phosphorylation and membrane translocation of protein kinase C ζ. Inhibitory protein kinase C ζ pseudosubstrate blocked S-nitroso-N-acetylpenicillamine-induced tight junction reorganization, but not myosin light chain phosphorylation. Epithelial inducible nitric oxide synthase activates two distinct signals, protein kinase C ζ and Rho-associated kinase, to disrupt tight junctions leading to bacterial influx.
Li-Ling Wu; Hsin-Da Chiu; Wei-Hao Peng; Bor-Ru Lin; Kuo-Shyan Lu; Yen-Zhen Lu; Linda Chia-Hui Yu. Epithelial inducible nitric oxide synthase causes bacterial translocation by impairment of enterocytic tight junctions via intracellular signals of Rho-associated kinase and protein kinase C zeta*. Critical Care Medicine 2011, 39, 2087 -2098.
AMA StyleLi-Ling Wu, Hsin-Da Chiu, Wei-Hao Peng, Bor-Ru Lin, Kuo-Shyan Lu, Yen-Zhen Lu, Linda Chia-Hui Yu. Epithelial inducible nitric oxide synthase causes bacterial translocation by impairment of enterocytic tight junctions via intracellular signals of Rho-associated kinase and protein kinase C zeta*. Critical Care Medicine. 2011; 39 (9):2087-2098.
Chicago/Turabian StyleLi-Ling Wu; Hsin-Da Chiu; Wei-Hao Peng; Bor-Ru Lin; Kuo-Shyan Lu; Yen-Zhen Lu; Linda Chia-Hui Yu. 2011. "Epithelial inducible nitric oxide synthase causes bacterial translocation by impairment of enterocytic tight junctions via intracellular signals of Rho-associated kinase and protein kinase C zeta*." Critical Care Medicine 39, no. 9: 2087-2098.
Inflammation and oxidative stress contribute to liver injury. Amla (Emblica officinalis Gaertn.) is rich in vitamin C, gallic acid, flavonoids, and tannins, which may protect against hepatoxicity-induced liver injury. We elucidated the effects of supplementary Amla (100 mg/kg of body weight) on N-nitrosodiethylamine-induced injury by evaluating reactive oxygen species (ROS) responses in the liver and bile, the degree of accumulated leukocytes and Kupffer cell infiltration, 3-nitrotyrosine and 4-hydroxynonenal stains, apoptosis and autophagy, plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT), and γ-glutamyl transpeptidase (γ-GT) levels, and antioxidant/oxidant enzymes in rats. Amla was more potent than vitamin C in scavenging O2−·, hydrogen peroxide, and nitric oxide. N-Nitrosodiethylamine increased ROS production in liver and bile, hepatic Kupffer cell and leukocyte infiltration, 3-nitrotyrosine and 4-hydroxynonenal accumulations, apoptosis and autophagy, and plasma ALT, AST, and γ-GT levels in the rats, decreased hepatic manganese superoxide dismutase (MnSOD) and catalase protein expressions, and enhanced inducible nitric oxide synthase (iNOS) and cytochrome P450 2E1 (CYP2E1) protein expressions. Amla significantly preserved MnSOD and catalase expressions and decreased iNOS and CYP2E1 protein expressions in N-nitrosodiethylamine-treated livers. Amla decreased N-nitrosodiethylamine-enhanced hepatic apoptosis and autophagy appearances via down-regulation of the Bax/Bcl-2 ratio and Beclin-1 expression. Thus Amla supplementation counteracts N-nitrosodiethylamine-induced liver injury via its antioxidant, anti-inflammation, anti-apoptosis, and anti-autophagy properties.
Kuo-Hsin Chen; Bor-Ru Lin; Chiang-Ting Chien; Chien-Hsin Ho. Emblica officinalisGaertn. AttentuatesN-Nitrosodiethylamine-Induced Apoptosis, Autophagy, and Inflammation in Rat Livers. Journal of Medicinal Food 2011, 14, 746 -755.
AMA StyleKuo-Hsin Chen, Bor-Ru Lin, Chiang-Ting Chien, Chien-Hsin Ho. Emblica officinalisGaertn. AttentuatesN-Nitrosodiethylamine-Induced Apoptosis, Autophagy, and Inflammation in Rat Livers. Journal of Medicinal Food. 2011; 14 (7-8):746-755.
Chicago/Turabian StyleKuo-Hsin Chen; Bor-Ru Lin; Chiang-Ting Chien; Chien-Hsin Ho. 2011. "Emblica officinalisGaertn. AttentuatesN-Nitrosodiethylamine-Induced Apoptosis, Autophagy, and Inflammation in Rat Livers." Journal of Medicinal Food 14, no. 7-8: 746-755.
Study Objective. To determine the factors that may influence Helicobacter pylori eradication in patients receiving omeprazole‐amoxicillin dual therapy.
Jyh-Chin Yang; Hong-Long Wang; Herng-Der Chern; Chia-Tung Shun; Bor-Ru Lin; Lin Chun-Jung; Teh-Hong Wang. Role of Omeprazole Dosage and Cytochrome P450 2C19 Genotype in Patients Receiving Omeprazole-Amoxicillin Dual Therapy for Helicobacter pylori Eradication. Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 2011, 31, 227 -238.
AMA StyleJyh-Chin Yang, Hong-Long Wang, Herng-Der Chern, Chia-Tung Shun, Bor-Ru Lin, Lin Chun-Jung, Teh-Hong Wang. Role of Omeprazole Dosage and Cytochrome P450 2C19 Genotype in Patients Receiving Omeprazole-Amoxicillin Dual Therapy for Helicobacter pylori Eradication. Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy. 2011; 31 (3):227-238.
Chicago/Turabian StyleJyh-Chin Yang; Hong-Long Wang; Herng-Der Chern; Chia-Tung Shun; Bor-Ru Lin; Lin Chun-Jung; Teh-Hong Wang. 2011. "Role of Omeprazole Dosage and Cytochrome P450 2C19 Genotype in Patients Receiving Omeprazole-Amoxicillin Dual Therapy for Helicobacter pylori Eradication." Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 31, no. 3: 227-238.
Chang MC, Chen YJ, Lee MY, Lin LD, Wang TM, Chan CP, Tsai YL, Wang CY, Lin BR, Jeng JH. Prostaglandin F2α stimulates MEK‐ERK signalling but decreases the expression of alkaline phosphatase in dental pulp cells. International Endodontic Journal, 43, 461–468, 2010. Abstract Aim To study prostaglandin F2α (PGF2α) receptor expression and downstream signalling in cultured human dental pulp cells and the effect of PGF2α on the alkaline phosphatase (ALP) activity of dental pulp cells. Methodology Human dental pulp cells were cultured and exposed to PGF2α. The expression of PGF2α (FP) receptors was analysed by reverse transcriptase polymerase chain reaction (RT‐PCR) and Western blotting. The activation of extracellular regulated kinase (ERK) and cAMP responsive element binding protein/activating transcription factor‐1 (CREB/ATF‐1) signalling was determined by Western blotting. The expression of ALP in pulp cells after exposure to PGF2α was evaluated by ALP staining and PCR. Results Dental pulp cells expressed FP receptor mRNA and protein. Exposure to PGF2α revealed little cytotoxicity to pulp cells. PGF2α induced both ERK and CREB/ATF‐1 phosphorylation in pulp cells. Exposure to PGF2α (>1 μmol L−1) further decreased the ALP activity and mRNA expression. However, U0126 (an inhibitor of MEK1) showed little preventive effect on the decline of ALP activity in dental pulp cells by PGF2α. Conclusion PGF2α may potentially activate FP receptors leading to ERK/CREB‐ATF‐1 activation during its production in inflamed dental pulp. PGF2α attenuated the ALP activity of pulp cells possibly via pathways not solely by MEK/ERK activation. PGF2α is a contributing factor of pulpal inflammation by regulating the activities of pulp cells.
M. C. Chang; Yi-Jane Chen; M. Y. Lee; Li-Deh Lin; Tong-Mei Wang; C. P. Chan; Yi-Ling Tsai; C. Y. Wang; Bor-Ru Lin; Jiiang-Huei Jeng. Prostaglandin F2α stimulates MEK-ERK signalling but decreases the expression of alkaline phosphatase in dental pulp cells. International Endodontic Journal 2010, 43, 461 -468.
AMA StyleM. C. Chang, Yi-Jane Chen, M. Y. Lee, Li-Deh Lin, Tong-Mei Wang, C. P. Chan, Yi-Ling Tsai, C. Y. Wang, Bor-Ru Lin, Jiiang-Huei Jeng. Prostaglandin F2α stimulates MEK-ERK signalling but decreases the expression of alkaline phosphatase in dental pulp cells. International Endodontic Journal. 2010; 43 (6):461-468.
Chicago/Turabian StyleM. C. Chang; Yi-Jane Chen; M. Y. Lee; Li-Deh Lin; Tong-Mei Wang; C. P. Chan; Yi-Ling Tsai; C. Y. Wang; Bor-Ru Lin; Jiiang-Huei Jeng. 2010. "Prostaglandin F2α stimulates MEK-ERK signalling but decreases the expression of alkaline phosphatase in dental pulp cells." International Endodontic Journal 43, no. 6: 461-468.
Oxidative stress and inflammation contributed to the propagation of acute liver injury (ALI). The present study was undertaken to determine whether D-galactosamine (D-GalN) induces ALI via the mitochondrial apoptosis- and proinflammatory cytokine-signaling pathways, and possible mechanism(s) by which green tea (GT) extract modulates the apoptotic and proinflammatory signaling in rat. D-GalN induced hepatic hypoxia/hypoperfusion and triggered reactive oxygen species (ROS) production from affected hepatocytes, infiltrated leukocytes, and activated Kupffer cells. D-GalN evoked cytosolic Bax and mitochondrial cytochrome C translocation and activated proinflammatory nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1) translocation, contributing to the increase of intercellular adhesion molecule-1 expression, terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL)-positive hepatocytes, multiple plasma cytokines and chemokines release, and alanine aminotransferase (ALT) activity. An altered biliary secretion profile of several acute phase proteins directly indicates oxidative stress affecting intracellular trafficking in the hepatocyte. GT pretreatment attenuated ROS production, mitochondrial apoptosis- and proinflammatory cytokine-signaling pathway, plasma ALT and cytokines levels, biliary acute phase proteins secretion and hepatic pathology by the enhancement of anti-apoptotic mechanisms. In conclusion, D-GalN induced ALI via hypoxia/hypoperfusion-enhanced mitochondrial apoptosis- and proinflammatory cytokine-signaling pathway, contributing to oxidative stress and inflammation in the liver. GT can counteract the D-GalN-induced ALI via the attenuation of apoptotic and proinflammatory signaling by the upregulation of anti-apoptotic mechanism.
Bor-Ru Lin; Chia-Jung Yu; Wang-Chuan Chen; Hsuan-Shu Lee; Huei-Min Chang; Yen-Chih Lee; Chiang-Ting Chien; Chau-Fong Chen. Green tea extract supplement reduces D-galactosamine-induced acute liver injury by inhibition of apoptotic and proinflammatory signaling. Journal of Biomedical Science 2009, 16, 35 -35.
AMA StyleBor-Ru Lin, Chia-Jung Yu, Wang-Chuan Chen, Hsuan-Shu Lee, Huei-Min Chang, Yen-Chih Lee, Chiang-Ting Chien, Chau-Fong Chen. Green tea extract supplement reduces D-galactosamine-induced acute liver injury by inhibition of apoptotic and proinflammatory signaling. Journal of Biomedical Science. 2009; 16 (1):35-35.
Chicago/Turabian StyleBor-Ru Lin; Chia-Jung Yu; Wang-Chuan Chen; Hsuan-Shu Lee; Huei-Min Chang; Yen-Chih Lee; Chiang-Ting Chien; Chau-Fong Chen. 2009. "Green tea extract supplement reduces D-galactosamine-induced acute liver injury by inhibition of apoptotic and proinflammatory signaling." Journal of Biomedical Science 16, no. 1: 35-35.
Background: Tongue cancer metastasis is mainly through blood stream and possibly associated with tumor cell‐induced platelet aggregation (TCIPA). Methods: Platelet aggregation was induced by different amounts of SAS tongue cancer cells with/without inhibitors and the latent period for induction of platelet aggregation was recorded. Gene expression was analyzed by reverse transcriptase‐polymerase chain reaction. Results: SAS cells (4 × 104 to 1 × 106 cells/ml) induced platelet aggregation in a cell density‐dependent manner. The latent period for induction of platelet aggregation reduced from 11.3 min (2 × 105 cells/ml) to 0.9 min (5 × 105 cells/ml). The extent of platelet aggregation increased from 39% to 76% by 2 × 105 and 5 × 105 SAS cells. Pre‐treatment of SAS cells with aspirin showed little effect on its induction of platelet aggregation. SAS cells expressed tissue factor (TF) mRNA and the SAS cells‐induced TCIPA was inhibited by TF neutralization antibody (5–20 μg/ml), heparin (5–10 U/ml), Hirudin fragment 54–65 (50 μg/ml) and D‐Phenylalanyl‐L‐prolyl‐L‐arginine chloromethyl ketone. But areca nut (AN, a betel quid component known to generate reactive oxygen species (ROS)) extract showed little effect on TF expression in SAS cells. Pre‐treatment with U73122 and 2‐aminoethoxydiphenylborate inhibited SAS‐induced TCIPA. Interestingly, catalase suppressed SAS cells‐induced TCIPA, whereas AN extract enhanced this event. Conclusions: These results suggest that tongue cancer cells may induce TCIPA and enhance tumor metastasis. SAS‐induced TCIPA is related to TF secretion, thrombin generation and associated with Phospholipase C‐Inositol triphosphate signaling and ROS production. Betel quid chewing may potentially promote tongue cancer metastasis.
Mei-Chi Chang; Chiu-Po Chan; Yuan-Soon Ho; Jang-Jaer Lee; Po-Shuen Lin; Bor-Ru Lin; Ya-Ling Huang; Liang-Jiunn Hahn; Hung-Wei Yeh; Ying-Jan Wang; Jiiang-Huei Jeng. Signaling pathways for induction of platelet aggregation by SAS tongue cancer cells - a mechanism of hematogenous metastasis. Journal of Oral Pathology & Medicine 2008, 38, 434 -440.
AMA StyleMei-Chi Chang, Chiu-Po Chan, Yuan-Soon Ho, Jang-Jaer Lee, Po-Shuen Lin, Bor-Ru Lin, Ya-Ling Huang, Liang-Jiunn Hahn, Hung-Wei Yeh, Ying-Jan Wang, Jiiang-Huei Jeng. Signaling pathways for induction of platelet aggregation by SAS tongue cancer cells - a mechanism of hematogenous metastasis. Journal of Oral Pathology & Medicine. 2008; 38 (5):434-440.
Chicago/Turabian StyleMei-Chi Chang; Chiu-Po Chan; Yuan-Soon Ho; Jang-Jaer Lee; Po-Shuen Lin; Bor-Ru Lin; Ya-Ling Huang; Liang-Jiunn Hahn; Hung-Wei Yeh; Ying-Jan Wang; Jiiang-Huei Jeng. 2008. "Signaling pathways for induction of platelet aggregation by SAS tongue cancer cells - a mechanism of hematogenous metastasis." Journal of Oral Pathology & Medicine 38, no. 5: 434-440.
Bor-Ru Lin; H T Hsieh; Jang-Ming Lee; I-Rue Lai; C F Chen; Linda Chia-Hui Yu. Luminal hydrochloric acid stimulates rapid transepithelial ion fluxes in rodent esophageal stratified squamous epithelium. Journal of physiology and pharmacology : an official journal of the Polish Physiological Society 2008, 59, 1 .
AMA StyleBor-Ru Lin, H T Hsieh, Jang-Ming Lee, I-Rue Lai, C F Chen, Linda Chia-Hui Yu. Luminal hydrochloric acid stimulates rapid transepithelial ion fluxes in rodent esophageal stratified squamous epithelium. Journal of physiology and pharmacology : an official journal of the Polish Physiological Society. 2008; 59 (3):1.
Chicago/Turabian StyleBor-Ru Lin; H T Hsieh; Jang-Ming Lee; I-Rue Lai; C F Chen; Linda Chia-Hui Yu. 2008. "Luminal hydrochloric acid stimulates rapid transepithelial ion fluxes in rodent esophageal stratified squamous epithelium." Journal of physiology and pharmacology : an official journal of the Polish Physiological Society 59, no. 3: 1.