Background: The aim of this study was to determine the effect of Sparstolonin B (SsnB) on cell proliferation and apoptosis in human breast cancer (MCF-7) and human ovarian epithelial cancer (OVCAR-3) cell lines in the presence and absence of estradiol hemihydrate (ES). Phosphoinositol-3 kinase (PI3K), phosphorylated protein kinase B alpha (p-AKT), phosphorylated mTOR (mechanistic target of rapamycin) signaling proteins, and sphingomyelin/ceramide metabolites were also measured within the scope of the study. Methods: The anti-proliferative effects of SsnB therapy were evaluated over a range of times and concentrations. Cell proliferation was determined by measuring the Proliferating Cell Nuclear Antigen (PCNA). PCNA was quantified by ELISA and cell distribution was assessed by immunofluorescence microscopy. MTT analysis was used to test the vitality of the cells, while LC-MS/MS was used to analyze the amounts of ceramides (CERs), sphingosine-1-phosphate (S1P), and sphingomyelins (SMs). TUNEL labeling was used to assess apoptosis, while immunofluorescence staining and enzyme-linked immunosorbent assay (ELISA) were used to measure the levels of PI3K, p-AKT, and p-mTOR proteins. Results: Sparstolonin B administration significantly decreased cell viability in MCF-7 and OVCAR-3 cells both in the presence and absence of ES, while it did not cause toxicity in healthy human fibroblasts. In comparison to controls, cancer cells treated with SsnB showed a significant drop in the levels of S1P, PI3K, p-AKT, and p-mTOR. In cancer cells cultured with SsnB, a significant increase in intracellular concentrations of C16-C24 CERs and apoptosis was observed. Conclusions: SsnB downregulated the levels of S1P, PI3K, p-AKT, and p-mTOR while reducing cell proliferation and promoting ceramide buildup and apoptosis.

Fibromyalgia Syndrome (FMS) is a chronic syndrome commonly characterized by widespread musculoskeletal pain and fatigue. Current evidence suggests that FMS diagnosis relies on clinical evaluation and patient-reported symptoms. MicroRNAs, which serve as key regulators of gene expression, have been proposed to play a role in the pathogenesis of FMS and other chronic pain syndromes. In this pilot study, miRNA-223-3p expression levels were examined in patients with FMS, and their relationship with pain intensity—assessed using the Visual Analog Scale (VAS)was evaluated. To obtain a broader understanding of the inflammatory response, serum interleukin-1 beta (IL-1β) levels were also measured. miRNA-223-3p expression levels were significantly reduced in the FMS group compared with healthy controls (p < 0.05), whereas IL-1β levels did not differ significantly between the groups (p = 0.1135). The negative correlation between miRNA-223-3p and VAS scores indicates that lower miRNA levels are associated with increased pain severity. Overall, these results suggest that reduced miRNA-223-3p expression levels may be linked to neuroimmune processes and heightened pain perception in FMS. The findings provide valuable preliminary insights that may guide future studies with larger sample sizes.

Asperglaucide (ASP) is an aurantiamide, an effective constituent of purslane (Portulaca oleraceaL.), a safe to eat greenery. Effects of ASP on endothelial function, endothelial nitric oxide synthase (eNOS) expression, vascular fluidity, renal and vascular reactive oxygen, and nitrogen species (ROS/RNS) production was examined in the two-kidney one-clip (2 K-1C) rat model of renovascular arterial hypertension. ASP toxicity, dose dependent eNOS gene expression and protein levels were also analyzed in human umbilical vein endothelial cells (HUVEC). The 2 K-1C model of hypertension was created via surgery and mean blood pressure (MBP) was measured by tail-cuff method during four weeks of ASP treatment. Erythrocyte deformability was monitored by rotational ektacytometry, while vascular constrictor and dilator responses were determined in organ baths. eNOS gene expression and protein levels were assessed in thoracic aorta and HUVEC. MBP was significantly decreased in hypertensive rats treated with ASP. Endothelium dependent vascular dilator and constrictor responses were also considerably improved following ASP treatment. There was a notable increase in red blood cell deformability in hypertensive rats treated with ASP as compared to hypertensive rats alone. A significant increase was observed in eNOS gene expression and protein levels in both normotensive and hypertensive rats treated with ASP. Treatment of HUVEC with 3 µM ASP notably increased eNOS mRNA and protein levels. In conclusion, ASP lowered blood pressure, improved endothelium-mediated relaxation, decreased renovascular ROS/RNS production in hypertensive rats. ASP also increased eNOS protein expression in aorta and HUVEC at nontoxic doses. ASP may have future potential as an anti-hypertensive agent.

This study aimed to compare the salivary galectin-3 and galectin-9 levels in periodontitis, gingivitis, and periodontally healthy patients. This study included 75 non-smokers who were systemically healthy. The clinical periodontal parameters of each participant were recorded. Individuals with periodontal health, gingivitis, and Stage II or Stage III Grade B periodontitis were allocated to the corresponding study groups (n = 25 each). Saliva samples were obtained from all individuals after they abstained from drinking and eating 1 h before sample collection. The galectin-3 and galectin-9 levels in the saliva were analyzed using enzyme-linked immunosorbent assay. One-way analysis of variance, student's t-test, Spearman correlation, and logistic regression were used for statistical analyses. The galectin-3 and galectin-9 levels were significantly higher in the periodontitis and gingivitis groups than in the healthy group (p < 0.001). The highest galectin-3 and galectin-9 levels were observed in the gingivitis group (p < 0.05). Overall, the galectin-3 levels were significantly higher than the galectin-9 levels in all the groups (p < 0.001). The salivary galectin-3 and galectin-9 levels were high in patients with periodontitis and gingivitis, suggesting that they could be potential biomarkers for periodontal diseases.

Background/Aim: Atherosclerosis is a chronic and progressive pathological condition marked by the accumulation of lipids, fibrous materials, and inflammatory cells, within the arterial walls. MicroRNAs (miRNAs) are single-stranded, evolutionarily conserved, non-coding small RNAs, that play a pivotal role in controlling various pathophysiological cellular functions and molecular signalling cascades associated with the development of atherosclerosis. Additionally, dysregulation in cholesterol and lipid metabolism is known to increase susceptibility to atherosclerosis. In this study, we aimed to determine the changes in serum levels of miRNA-199a-5p, examine its relationship with LDL cholesterol, and investigate its diagnostic value in patients diagnosed with atherosclerosis. Materials and Methods: MiRNA-199a-5p expression analysis was conducted using PCR on serum samples from 20 patients diagnosed with atherosclerosis and 26 completely healthy, voluntary control subjects. The blood biochemical analysis values for all groups participating in the study were obtained from their records. Results: The data analysis revealed significant up-regulation of miRNA-199a-5p in the serum of the patient group. Additionally, miRNA-199a-5p expression levels positively correlated with LDL cholesterol levels. Conclusion: miRNA-199a-5p can be considered a reliable biomarker in patients with atherosclerosis, potentially informing and guiding future therapeutic approaches. Additionally, a significant relationship was found between lipid metabolism and miRNA-199a-5p in atherosclerosis.