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目的:探讨党参炔苷对雌性大鼠卵巢颗粒细胞(GCs)增殖分化的影响及其作用机制。方法:观察大鼠卵巢GCs的生长状况,通过CCK-8实验和细胞雌二醇(E2)分泌量测定确定细胞体外培养时间以及最佳给药浓度,进一步观察党参炔苷对体外培养的卵巢GCs增殖分化及分泌功能的影响,并通过阻断GCs中的c AMP信号通路、ERK 1/2信号通路、p38MAPK信号通路和钙离子(Ca2+)通道来探究其对卵巢GCs功能影响的作用机制。结果:确定24 h为GCs最佳共培养时间;党参炔苷浓度为3.125 mg/L时,能显著增加E2的分泌量(P<0.01),对细胞3β-羟基固醇脱氢酶(3β-HSD)含量和CCK-8实验吸光度(D)值均无影响(P>0.05)。c AMP通路抑制剂H89和p38MAPK通路抑制剂SB203580能够抑制党参炔苷对卵巢GCs分泌E2的促进作用(P<0.01)。结论:党参炔苷可有效促进卵巢GCs分泌E2,且不影响细胞的增殖和正常分化;党参炔苷可能通过c AMP和p38MAPK信号通路来促进GCs对E2的合成及分泌。
Objective: To investigate the effects of Codonopynin on the proliferation and differentiation of ovarian granulosa cells (GCs) in female rats and its mechanism. Methods: The growth of ovary GCs in rats was observed. The cell culture time and the best administration concentration were determined by CCK-8 assay and the secretion of estradiol (E2) in cells. The effects of Codonopynin on ovary GCs Proliferation, differentiation and secretion of GCs, and to explore its mechanism of action on ovarian GCs by blocking the cAMP signaling pathway, ERK 1/2 signaling pathway, p38MAPK signaling pathway and calcium ion (Ca 2+) channel in GCs. Results: 24 h was the best co-culture time for GCs. When the concentration of Codonaponin was 3.125 mg / L, the secretion of E2 was significantly increased (P <0.01), the 3β-hydroxysteroid dehydrogenase HSD) content and CCK-8 experimental absorbance (D) values had no effect (P> 0.05). c AMP pathway inhibitor H89 and p38MAPK pathway inhibitor SB203580 can inhibit the promotion of E2 of E2 induced by GCs (P <0.01). CONCLUSION: Codonopsis glycosides can effectively promote the secretion of E2 from ovarian GCs without affecting the proliferation and normal differentiation of cells. Cod -in may promote the synthesis and secretion of E2 by GCs through the cAMP and p38 MAPK signaling pathways.