加味四君子汤调控PI3K/AKT/FoxO1信号通路对CTX诱导卵巢早衰大鼠的作用机制研究OA
Regulation of the PI3K/AKT/FoxO1 signaling pathway by Jiawei Sijunzi Decoction(加味四君子汤)in alleviating cyclophosphamide-induced premature ovarian failure in rats
目的 探讨加味四君子汤通过调控PI3K/AKT/FoxO1信号通路对环磷酰胺(CTX)诱导的卵巢早衰(POF)大鼠的作用机制.方法 选取50只大鼠编号,随机分为空白组(10只)和造模组(40只).造模组以腹腔注射CTX构建POF模型,建模成功后将大鼠再随机分为模型组、加味四君子汤低、中、高剂量组(各10只).采用ELISA法检测血清FSH、LH、E₂、AMH、GnRH水平,HE染色观察卵巢组织形态学改变,Western blot检测卵巢组织PI3K、Akt、FoxO1、Bcl-2、Caspase-3、Bax蛋白表达水平,q-PCR法检测卵巢组织PI3K、Akt、FOXO1 mRNA表达情况.结果 与空白组相比,模型组卵泡闭锁数、FSH、LH、Bax、Caspase-3、PI3K/p-PI3K、AKT/p-AKT及其mRNA和蛋白表达水平均升高(P均<0.05),E₂、AMH、Bcl-2、FoxO1及其mRNA和蛋白表达水平均降低(P均<0.05).与模型组相比,加味四君子汤各剂量组上述指标变化趋势相反(P均<0.05).结论 加味四君子汤可能通过调控PI3K/Akt/FoxO1信号通路,改善卵巢组织形态,减少卵泡过度闭锁与耗竭,进而改善CTX诱导的卵巢早衰.
Objective To investigate the mechanism by which Jiawei Sijunzi Decoction(加味四君子汤,JSD)alleviates cyclophospha-mide(CTX)-induced premature ovarian failure(POF)in rats through regulation of the PI3K/AKT/FoxO1 signaling pathway.Methods Fifty rats were numbered and randomly divided into a blank group(n=10)and a model control group(n=40).The POF model was estab-lished by intraperitoneal injection of CTX.After successful modeling,the model rats were randomly divided into model group,low/medium/high-dose JSD groups(n=10 each).Serum levels of follicle-stimulating hormone(FSH),luteinizing hormone(LH),estradiol(E2),anti-Müllerian hormone(AMH),and gonadotropin-releasing hormone(GnRH)were measured by ELISA.Ovarian tissue mor-phology was observed by HE staining.Protein expression levels of PI3K,AKT,FoxO1,Bcl-2,Caspase-3,and Bax in ovarian tissues were detected by Western blot(WB).mRNA expression levels of PI3K,AKT,and FoxO1 in ovarian tissues were detected by q-PCR.Results Compared with the blank group,the number of atretic follicles,serum FSH and LH levels,as well as the protein and mRNA expression levels of PI3K,p-PI3K,AKT,p-AKT,Bax,and Caspase-3 in the model group were significantly increased(all P<0.05),while serum E2 and AMH levels,and the protein and mRNA expression levels of Bcl-2 and FoxO1 were significantly decreased(all P<0.05).Compared with the model group,the above indexes in the JSD dose groups showed the opposite trend(all P<0.05).Conclusion JSD may alleviate CTX-induced premature ovarian failure by regulating the PI3K/AKT/FoxO1 signaling pathway,ameliorating ovarian tissue morphology and reducing excessive follicular atresia and depletion.
桑玉莹;辛如娟;代雅婷;李晶;王新斌
甘肃中医药大学中西医结合学院,甘肃 兰州 730000甘肃中医药大学中西医结合学院,甘肃 兰州 730000甘肃中医药大学中西医结合学院,甘肃 兰州 730000甘肃中医药大学中西医结合学院,甘肃 兰州 730000甘肃中医药大学中西医结合学院,甘肃 兰州 730000
医药卫生
PI3K/AKT/FoxO1信号通路加味四君子汤卵巢早衰环磷酰胺
PI3K/AKT/FoxO1 signaling pathwayJiawei Sijunzi Decoction(加味四君子汤)Premature ovarian failureCyclo-phosphamide
《时珍国医国药》 2026 (17)
3244-3249,6
甘肃省自然科学基金(23JRRA1206)
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