目的 探讨地榆皂苷Ⅱ通过PI3K/Akt/mTOR通路对链脲佐菌素诱导的大鼠视网膜病变的影响。方法 通过ip链脲佐菌素35 mg/kg建立糖尿病大鼠模型，通过高糖诱导的Müller细胞建立糖尿病细胞模型。采用ELISA法检测血清、视网膜和细胞上清液中细胞因子水平。采用试剂盒检测血清胰岛素和口服葡萄糖耐量（OGTT）、血清超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量。通过苏木精-伊红（HE）染色评估视网膜组织的病理变化。采用Western blotting检测糖尿病小鼠视网膜组织和高糖诱导的Müller细胞中的磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（Akt）/哺乳动物雷帕霉素靶蛋白（mTOR）信号通路蛋白表达水平。结果 与模型组相比，地榆皂苷Ⅱ显著降低血清胰岛素水平并改善OGTT；显著增加血清、视网膜和Müller细胞中的SOD并降低MDA水平。地榆皂苷Ⅱ还显著降低糖尿病大鼠和高糖诱导的Müller细胞中的血清和视网膜细胞因子。结论 地榆皂苷Ⅱ可抑制视网膜组织和高糖诱导的Müller细胞中的PI3K/Akt/mTOR信号通路，从而改善糖尿病视网膜病变。

Objective To explore the effect of ziyuglycoside II on diabetic retinopathy in streptozotocin-induced rats based on PI3K/ Akt/mTOR pathway. Methods Rat model of diabetic retinopathy was established by intraperitoneal injection of streptozotocin 35mg/kg. Cell model of diabetic retinopathy was established by glucose-induced Müller cell. The levels of cytokines in serum, retina and cell supernatant were detected by ELISA. Serum insulin and OGTT, serum SOD activity and MDA content were measured by the kit. The pathological changes of retinal tissue were evaluated by HE staining. Western blotting was used to detect the PI3K/Akt/mTOR signaling pathway in retinal tissues of diabetic mice and Müller cells induced by high glucose. Results Compared with model group, ziyuglycoside II significantly decreased serum insulin level and improved OGTT. SOD levels in serum, retina and Müller cells were significantly increased and MDA levels were decreased. ziyuglycoside II also significantly reduced serum and retinal cytokines in diabetic rats and high-sugar-induced Müller cells. Conclusions Ziyuglycoside II could inhibited PI3K/Akt/mTOR signal pathway in retina tissue and glucose-induced Müller cell. ziyuglycoside II may improve retinopathy in diabetic retinopathy, oxidative stress and inflammation in the retina tissue of rats and glucose-induced Müller cell.

R285.5

河南省科技攻关计划项目(242102311261);河南省高等学校重点科研项目(23A360018)