【摘要】 目的 探讨硫化氢（H2S）对需氧菌性阴道炎的作用及其分子机制。方法 使用大肠埃希菌（E. coli）和金黄色葡萄球菌（S. aureus）感染分别制备细胞（VK2/E6E7）和大鼠需氧菌性阴道炎模型。硫氢化钠（NaHS）被用为H2S供体。采用CCK-8、蛋白印迹、qPCR和流式细胞术等分别检测细胞活性、蛋白表达、mRNA表达和细胞内氯离子水平。结果 E. coli和S. aureus感染促进VK2/E6E7细胞和阴道组织中IL-6和IL-1β的生成，NaHS能显著抑制这些促炎细胞因子的产生。NaHS显著抑制E. coli或S. aureus感染引起的NF-κB(p65)磷酸化。NaHS显著降低E. coli和S. aureus感染阴道上皮细胞内的氯离子浓度。结论 H2S可能通过降低细胞内氯离子浓度而抑制NF-κB信号通路的激活，从而抑制E. coli和S. aureus感染引起的阴道炎症反应。H2S可开发成为治疗需氧菌性阴道炎的潜在药物。更多还原

【Abstract】 Objective To investigate the effect and molecular mechanism of hydrogen sulfide(H2S) on inflammatory responses in aerobic vaginitis(AV). Methods Escherichia coli(E. coli) and Staphylococcus aureus(S. aureus) were used to establish cellular and rat AV models. Sodium hydrosulfide hydrate(NaHS) was used as an H2S donor. CCK-8, western blot, q PCR, and flow cytometry were employed to detemine cell viability, protein and mRNA expression,and intracellular Cl-concentration, respectively. Results Both E. coli and S. aureus infection significantly promoted the production of IL-6 and IL-1β in VK2/E6E7 cells and vaginal tissues, whereas NaHS treatment reduced the production of these proinflammatory cytokines in AV cells and vaginal tissues. NaHS treatment significantly reduced phosphorylated NF-κB(p65) induced by E. coli or S. aureus infection. Furthermore, NaHS treatment inhibited E.coli-and S. aureus-induced intracellular Cl-accumulation in vaginal epithelial cells. Conclusion H2S can inducing vaginal inflammatory responses in AV induced by E. coli and S. aureus infection, at least partially inducing intracellular Cl-accumulation and inhibiting the NF-κB signal pathway. H2S might serve as a potential drug for treating AV.更多还原