目的 探討地榆皂苷Ⅱ通過PI3K/Akt/mTOR通路對鏈脲佐菌素誘導的大鼠視網(wǎng)膜病變的影響。方法 通過ip鏈脲佐菌素35 mg/kg建立糖尿病大鼠模型，通過高糖誘導的Müller細胞建立糖尿病細胞模型。采用ELISA法檢測血清、視網(wǎng)膜和細胞上清液中細胞因子水平。采用試劑盒檢測血清胰島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。通過蘇木精-伊紅（HE）染色評估視網(wǎng)膜組織的病理變化。采用Western blotting檢測糖尿病小鼠視網(wǎng)膜組織和高糖誘導的Müller細胞中的磷脂酰肌醇3-激酶（PI3K）/蛋白激酶B（Akt）/哺乳動物雷帕霉素靶蛋白（mTOR）信號通路蛋白表達水平。結果 與模型組相比，地榆皂苷Ⅱ顯著降低血清胰島素水平并改善OGTT；顯著增加血清、視網(wǎng)膜和Müller細胞中的SOD并降低MDA水平。地榆皂苷Ⅱ還顯著降低糖尿病大鼠和高糖誘導的Müller細胞中的血清和視網(wǎng)膜細胞因子。結論 地榆皂苷Ⅱ可抑制視網(wǎng)膜組織和高糖誘導的Müller細胞中的PI3K/Akt/mTOR信號通路，從而改善糖尿病視網(wǎng)膜病變。

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

河南省科技攻關計劃項目(242102311261);河南省高等學校重點科研項目(23A360018)