Fang Yuwei, Shi Kangpei, Lu Haining, Lu Lin, Qiu Bo
Department of Ophthalmology, The Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou, China.
State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Front Pharmacol. 2021 Apr 13;12:632040. doi: 10.3389/fphar.2021.632040. eCollection 2021.
To investigate the effect of Mingmu Xiaomeng tablets (MMXM) on the expression of phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR)-related proteins in a diabetic rat model. Thirty-two male Sprague Dawley rats were randomly divided into four groups: normal control (NC), diabetic model (DM) control, MMXM, and calcium dobesilate (CD) Rats injected with streptozotocin (STZ) were used as an experimental diabetes model. After 14 weeks, autophagy and PI3K/Akt/mTOR signaling pathway proteins were detected by western blot. Glial fibrillary acidic protein (GFAP) expression in Müller cells was examined by immunohistochemistry. Retinal function was evaluated with electroretinography, and retinal ultrastructure was observed by transmission electron microscopy. Serum cytokine levels were detected with protein chip technology. MMXM restored autophagy by decreasing the protein expression of LC3-II and p62 and reducing the phosphorylation of PI3K, Akt, and mTOR, thus promoting autophagy. MMXM decreased GFAP expression in retinal Müller cells; restored electrophysiology indexes and retinal ultrastructures; and reduced serum levels of interleukin (IL)-1β, IL-4, IL-6, tumor necrosis factor-α, and vascular endothelial growth factor. MMXM may protect the diabetic retina by inhibiting PI3K/Akt/mTOR signaling and enhancing autophagy.
探讨明目消朦片（MMXM）对糖尿病大鼠模型中磷酸肌醇3激酶（PI3K）/蛋白激酶B（Akt）/雷帕霉素哺乳动物靶蛋白（mTOR）相关蛋白表达的影响。将32只雄性Sprague Dawley大鼠随机分为四组：正常对照组（NC）、糖尿病模型对照组（DM）、明目消朦片组和羟苯磺酸钙（CD）组。注射链脲佐菌素（STZ）的大鼠用作实验性糖尿病模型。14周后，通过蛋白质印迹法检测自噬及PI3K/Akt/mTOR信号通路蛋白。通过免疫组织化学法检测Müller细胞中胶质纤维酸性蛋白（GFAP）的表达。用视网膜电图评估视网膜功能，并用透射电子显微镜观察视网膜超微结构。用蛋白质芯片技术检测血清细胞因子水平。明目消朦片通过降低LC3-II和p62的蛋白表达以及减少PI3K、Akt和mTOR的磷酸化来恢复自噬，从而促进自噬。明目消朦片降低视网膜Müller细胞中GFAP的表达；恢复电生理指标和视网膜超微结构；并降低血清白细胞介素（IL）-1β、IL-4、IL-6、肿瘤坏死因子-α和血管内皮生长因子水平。明目消朦片可能通过抑制PI3K/Akt/mTOR信号传导和增强自噬来保护糖尿病视网膜。
