首页|期刊导航|广东医学|人参皂苷Rg3对LPS诱导颗粒细胞炎症的作用及机制研究

人参皂苷Rg3对LPS诱导颗粒细胞炎症的作用及机制研究OA

Effects of ginsenoside Rg3 on LPS-induced inflammation in ovarian granulosa cells and its underlying mecha-nisms

中文摘要英文摘要

目的 探讨人参皂苷Rg3对脂多糖(LPS)诱导的卵巢颗粒细胞炎症反应及凋亡的抑制作用,并分析其潜在分子机制.方法 分离培养C57BL/6小鼠原代卵巢颗粒细胞,建立LPS诱导的炎症模型.实验分为对照组、LPS组和LPS+Rg3干预组.采用CCK-8法检测细胞活力以确定Rg3的安全干预浓度;通过蛋白质免疫印迹(Western blot)检测NF-κB信号通路关键蛋白(p-p65、IκBα)、炎症蛋白COX-2及凋亡相关蛋白(Bel-2、Bax、Cleaved Caspase-3)的表达;利用实时定量PCR(qRT-PCR)检测炎症因子(IL-6、TNF-α、IL-1 β)的mRNA水平.结果 研究发现1 μmol/L Rg3对颗粒细胞毒性最小,且能有效逆转LPS引发的炎症与凋亡.LPS刺激显著激活了 TLR4和NF-κB通路(p-p65水平升高,IκBα降解),并上调了COX-2、IL-6(t=18.76,P<0.001)、TNF-α(t=15.42,P<0.001)、IL-1β(t=17.35,P<0.001)的表达,同时诱导线粒体凋亡途径(Bax/Bcl-2比率升高,Cleaved Caspase-3增加).而Rg3干预可显著抑制TLR4及NF-κB 通路的活化,降低促炎因子表达(IL-6:t=12.34,P<0.001;TNF-α:t=11.82,P<0.001;IL-1β:t=12.96,P<0.001),并有效逆转促凋亡蛋白与抗凋亡蛋白的比例.结论 人参皂苷Rg3能够通过TLR4途径抑制NF-κB信号通路,减轻LPS诱导的卵巢颗粒细胞炎症反应与凋亡.这为将Rg3开发为治疗卵巢炎症相关疾病(如多囊卵巢综合征)的潜在天然药物提供了重要的实验依据.

Objective To investigate the inhibitory effects of ginsenoside Rg3 on lipopolysaccharide(LPS)-in-duced inflammatory responses and apoptosis in ovarian granulosa cells,and to explore the underlying molecular mecha-nisms.Methods Primary ovarian granulosa cells were isolated from C57BL/6 mice and cultured in vitro to establish an LPS-induced inflammation model.Cells were divided into three groups:control group,LPS group,and LPS+Rg3 treat-ment group.Cell viability was assessed using the Cell Counting Kit-8(CCK-8)assay to determine the optimal non-toxic concentration of Rg3.Protein expression levels of key components in the NF-κB signaling pathway(p-p65 and IκBα),the inflammatory mediator COX-2,and apoptosis-related proteins(Bel-2,Bax,and cleaved caspase-3)were analyzed by Western blotting.mRNA expression levels of inflammatory cytokines(IL-6,TNF-α,and IL-1 β)were quantified by real-time quantitative PCR(qRT-PCR).Results Rg3 at a concentration of 1 μmol/L exhibited minimal cytotoxicity and significantly attenuated LPS-induced inflammation and apoptosis in granulosa cells.LPS stimu-lation markedly activated the TLR4/NF-κB signaling pathway,as evidenced by increased p-p65 levels and degradation of IκBα,along with upregulation of COX-2,IL-6(t=18.76,P<0.001),TNF-α(t=15.42,P<0.001),and IL-1β(t=17.35,P<0.001)expression.Additionally,LPS induced mitochondrial apoptosis,as indicated by an in-creased Bax/Bcl-2 ratio and elevated levels of cleaved caspase-3.Treatment with Rg3 significantly inhibited the activa-tion of the TLR4/NF-κB pathway,reduced pro-inflammatory cytokine expression(IL-6:t=12.34,P<0.001;TNF-α:t=11.82,P<0.001;IL-1 β:t=12.96,P<0.001),and reversed the imbalance between pro-apoptotic and anti-apoptotic proteins.Conclusion This study demonstrates for the first time that ginsenoside Rg3 suppresses LPS-induced inflammation and apoptosis in ovarian granulosa cells by inhibiting the TLR4-mediated NF-κB signaling pathway.These findings provide important experimental evidence supporting the potential development of Rg3 as a natural therapeutic agent for ovarian inflammatory disorders,such as polycystic ovary syndrome(PCOS).

张露;彭伟;彭天雨;邓玲;韩艳

宜春市妇幼保健院辅助生殖科(江西宜春 336000)宜春市妇幼保健院辅助生殖科(江西宜春 336000)宜春市妇幼保健院辅助生殖科(江西宜春 336000)宜春市妇幼保健院辅助生殖科(江西宜春 336000)宜春市妇幼保健院辅助生殖科(江西宜春 336000)

医药卫生

人参皂苷Rg3卵巢颗粒细胞炎症凋亡NF-κB通路多囊卵巢综合征

ginsenoside Rg3ovarian granulosa cellsinflammationapoptosisNF-κB pathwaypolycystic ovary syndrome

《广东医学》 2026 (5)

666-671,6

中国江西省宜春市科技局科技项目(JXCY2025KSA135)

10.13820/j.cnki.gdyx.20254027

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