Oxidative stress and inflammation are hypothesized to contribute to the pathogenesis of chronic obstructive pulmonary disease (COPD). Resveratrol (trans-3,5,4′-trihydroxystilbene) is known for its antioxidant and anti-inflammatory properties. The study aimed to investigate the effects of resveratrol in a rat model with COPD on the regulation of oxidative stress and inflammation via the activation of Sirtuin1 (SIRTl) and proliferator-activated receptor-γ coactivator-1α (PGC-1α). Thirty Wistar rats were randomly divided into three groups: control group, COPD group and resveratrol intervention group. The COPD model was established by instilling with lipopolysaccharide (LPS) and challenging with cigarette smoke (CS). The levels of interleukin-6 (IL-6) and interleukin-8 (IL-8) in serum were measured. The levels of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) were measured. The expression levels of SIRT1 and PGC-1α in the lung tissues were examined by immunohistochemistry as well as real-time reverse transcriptase polymerase chain reaction (real-time RT-PCR) and western blotting analysis. After the treatment with resveratrol (50 mg/kg), compared with the COPD group, alleviation of inflammation and reconstruction in the small airways of the lungs were seen. Resveratrol might be correlated not only with the lower level of MDA and the higher activity of SOD, but also with the upregulation of SIRT1 and PGC-1α expression. Resveratrol treatment decreased serum levels of IL-6 and IL-8. Our findings indicate that resveratrol had a therapeutic effect in our rat COPD model, which is related to the inhibition of oxidative stress and inflammatory response. The mechanism may be related to the activation and upgrading of the SIRT1/PGC-1α signaling pathways. Thus resveratrol might be a therapeutic modality in COPD.

Oxidative stress is hypothesized to contribute to the pathogenesis of chronic obstructive pulmonary disease (COPD).The study was purposed to investigate the effects of resveratrol (trans-3,5,4'-trihydroxystilbene) in a rat model with COPD on the regulation of oxidative stress via the activation of Sirtuin1 (SIRTl) and proliferator-activated receptor-γ coactivator-1α (PGC-1α).Thirty Wistar rats were randomly divided into three groups: control group, COPD group and resveratrol intervention group. The model of COPD was established by instilling with lipopolysaccharide (LPS) and challenging with cigarette smoke (CS). The pathological changes in lungs were evaluated by hematoxylin and eosin (HE) stain. The levels of interleukin-6 (IL-6) and interleukin-8 (IL-8) in serum were measured by enzyme-linked immunosorbent assay (ELISA). The level of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in both lung tissue homogenate and bronchial alveolar lavage fluid (BALF) were examined by using the commercially available kits. The expression levels of SIRT1 and PGC-1α in the lung tissues were examined by immunohistochemistry as well as real-time reverse transcriptase polymerase chain reaction (real-time RT-PCR) and western blotting analysis. After the treatment with resveratrol (50mg/kg), compared with the COPD group, the alleviation of inflammation and the reconstruction in the small airways of lungs were seen, which might be correlated not only with the lower level of MDA and the higher activity of SOD, but also with the upregulation of SIRT1 and PGC-1α expression. Resveratrol treatment also decreased serum levels of IL-6 and IL-8. The results indicated that resveratrol appeared to reduce oxidative stress by altering the levels of MDA and SOD in our rat COPD model, and the possible mechanism of this intervention effect of resveratrol with COPD may be associated with its upregulation of SIRT1and PGC-1α.Thus resveratrol might be a therapeutic modality in COPD.

Objective: High-risk human papillomavirus (HR-HPV) screening has increased colposcopy referrals, particularly for women with HR-HPV positivity but no intraepithelial lesion or malignancy (NILM) and those with atypical squamous cells of undetermined significance (ASC-US). A fraction of low-grade squamous intraepithelial lesions (LSILs) is associated with cervical intraepithelial neoplasia grade 2 or worse (CIN2+) during diagnosis. This study evaluated the ability of GYPC methylation (GYPC^m) to distinguish between <CIN2 and CIN2 + in HPV-positive women with NILM, ASC-US, and LSIL cytology. It also assessed the absolute CIN2+/CIN3 + risk of the triage strategies GYPC^m, HPV genotyping, and their combination and compared the clinical performance of each triage strategy.Methods: To improve cervical screening efficiency, risk stratification based on HPV genotyping and GYPC^m was used as a triage strategy.Results: GYPC^m distinguished between 0.999) and significant differences in specificity (70.5% vs. 21.8%, p < 0.001). The HPV16/18 or GYPC^m triage strategy required the least number of referrals to detect a CIN2 + at 3.9 (3.3–4.6).Conclusion: HPV16/18 or GYPC^m as a triage tool in HPV-positive women with NILM, ASC-US, and LSIL cytology significantly reduced colposcopy referrals while maintaining sensitivity similar to that of HPV16/18 or ASC-US+.