Bcl-2 Recombinant Mouse Monoclonal Antibody [M43D02]

Oligoasthenospermia (OAS), a major cause of male infertility, was alleviated by Guilu-Erxian-Glue (GLEXG) in Tripterygium wilfordii polyglycoside (TWG)-induced rat models. This study identified GLEXG's bioactive ingredients and explored its therapeutic mechanism. Using network pharmacology and liquid chromatography-mass spectrometry, quercetin was predicted and validated as a key component of GLEXG. In vivo and in vitro, OAS models were established using TWG in mice and H 2 O 2 in spermatocytes. TWG administration reduced testicle and epididymis indices, sperm concentration, vitality, and serum testosterone, luteinizing hormone, and follicle-stimulating hormone. It also increased germ cell apoptosis, upregulated Bax, cleaved caspase-3, and cleaved caspase-9, downregualted Bcl-2, PHB1, VDHC, SDHA, and CoxIV, and impaired mitochondrial function (reduced mitochondrial DNA copy number and membrane potential). Quercetin counteracted these effects in vivo and in vitro. Mechanistically, quercetin increased p-PKA/PKA and p-CREB/CREB ratios, upregulated Sirt1, and decreased Ac-p53/p53 ratio. These beneficial effects were abolished upon Sirt1 inhibition. Thus, quercetin in GLEXG ameliorated OAS by attenuating apoptosis and mitochondrial dysfunction via PKA/CREB pathway-dependent activation of Sirt1 and deacetylation of p53.

Background Ferroptosis plays a key role in the development of chronic obstructive pulmonary disease (COPD). Whether ginsenoside Rg1 improves cigarette smoke-induced COPD or whether ginsenoside Rg1 improves COPD by inhibiting ferroptosis remains unknown. Methods BEAS-2B cells were exposed to cigarette solution (CSE) for 24 hours and treated with ginsenoside Rg1, the ferroptosis inhibitor Fer-1, and the PERK inhibitor GSK. Cell viability, endoplasmic reticulum stress, mitochondrial morphology, membrane potential, reactive oxygen species (ROS), iron levels, and the expression of related proteins were detected using corresponding methods. A COPD mouse model was constructed using cigarette smoke (CS). Ginsenoside Rg1 and GSK were administered via tube feeding 15 days after successful modeling. Mouse lung tissues were evaluated by HE staining. The expression of inflammatory markers, ROS, iron content, and related proteins was detected using corresponding methods. Results The results demonstrated that in the CSE-exposed BEAS-2B cell model and CS-induced mouse COPD model, the expression levels of endoplasmic reticulum stress (ERS)-related factors such as GRP78 were increased, while those of the antioxidant markers GPX4 and GSH were significantly decreased. Ginsenoside Rg1 improved emphysema and inflammation by inhibiting ferroptosis in vivo and in vitro. Using a PERK inhibitor, we found that ginsenoside Rg1 inhibited ferroptosis in vivo and in vitro by regulating ERS. Conclusion This study showed that ginsenoside Rg1 alleviates cigarette smoke-induced COPD by regulating the PERK/ATF4 axis to inhibit ERS and ferroptosis.