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作 者:李泉洋 靳英英 杜国辉 王楚王文 吴国泰 王瑞琼 LI Quanyang;JIN Yingying;DU Guohui;WANG Chuwangwen;WU Guotai;WANG Ruiqioong(College of Pharmacy,Gansu University of Chinese Medicine,Lanzhou,Gansu,730000 P.R.China;Key Laboratory of Pharmacology and Toxicology for TCM of Gansu Province,Gansu University of Chinese Medicine,Lanzhou,Gansu,730000 P.R.China)
机构地区:[1]甘肃中医药大学药学院,甘肃兰州730000 [2]甘肃中医药大学甘肃省中药药理与毒理学重点实验室,甘肃兰州730000
出 处:《华西药学杂志》2024年第5期497-502,共6页West China Journal of Pharmaceutical Sciences
基 金:国家自然科学基金资助项目(批准号:81660653);甘肃省青年博士基金项目(2021QB-074);甘肃省自然科学基金项目(22JR5RA588)。
摘 要:目的研究防风通圣散对多囊卵巢综合征(PCOS)小鼠的治疗作用及其机制。方法采用高脂饲料饲养与ig来曲唑1.4 mg·kg^(-1)建立小鼠PCOS模型,收集经防风通圣散治疗后模型小鼠的血液与卵巢组织,用于生化、病理与免疫学检测。采用网络药理学方法分析防风通圣散治疗PCOS的潜在靶点。结果防风通圣散可显著降低PCOS小鼠的空腹血糖水平,增加卵巢组织中黄体的数量与颗粒细胞层的厚度,上调血清中雌二醇、促卵泡激素的水平,降低白介素-6(IL-6)的水平;上调卵巢组织中蛋白激酶B(AKT)的表达,下调血管内皮生长因子(VEGF)A的表达。网络药理学分析显示:AKT、IL-6、VEGFA为防风通圣散治疗PCOS的核心靶点。结论防风通圣散可改善PCOS小鼠的卵巢病理损伤与激素紊乱症状,其机制与调控AKT、IL-6、VEGF的表达有关。OBJECTIVE To investigate the therapeutic effects and mechanism of Fangfeng Tongsheng powder(FTP)on mice with polycystic ovarian syndrome(PCOS).METHODS The PCOS mice model was established by feeding a high-fat diet with gavage Letrozole 1.4 mg·kg^(-1).Blood and ovarian tissue from model mice treated with FTP were collected for the biochemical,pathological and immunological tests.The potential targets of FTP for the treatment of PCOS were analyzed by Network pharmacology.RESULTS FTP significantly reduced the fasting blood glucose level,increased the number of corpus luteum and the thickness of granulosa cell layer in ovarian tissues,up-regulated the levels of estradiol and follicle stimulating hormone,and reduced the level of IL-6 in the serum of PCOS mice.It also up-regulated the expression level of AKT and down-regulated the expression level of VEGFA in ovarian tissues.Network pharmacological analysis showed that AKT,IL-6 and VEGFA are the core targets of FTP in the treatment of PCOS.CONCLUSION FTP can improve the pathological damage of ovarian tissues and hormone disorders in PCOS mice,and its mechanism is related to the regulation of AKT,IL-6 and VEGF expression.
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