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微小RNA-211通过靶向糖尿病性白内障小鼠中的基因对晶状体上皮细胞增殖和凋亡的影响

Effects of microRNA-211 on proliferation and apoptosis of lens epithelial cells by targeting gene in diabetic cataract mice.

作者信息

Zeng Kun, Feng Qi-Gao, Lin Bao-Tao, Ma Da-Hui, Liu Chun-Min

机构信息

Shenzhen Key Laboratory of Ophthalmology, Shenzhen Eye Hospital, Ophthalmology College of Shenzhen University, Shenzhen 518000, P.R. China

Shenzhen Key Laboratory of Ophthalmology, Shenzhen Eye Hospital, Ophthalmology College of Shenzhen University, Shenzhen 518000, P.R. China.

出版信息

Biosci Rep. 2017 Jul 27;37(4). doi: 10.1042/BSR20170695. Print 2017 Aug 31.

Abstract

Our study aimed at exploring the effects of on the proliferation and apoptosis of lens epithelial cells in diabetic cataract mice by targetting NAD-dependent histone deacetylase sirtulin 1 (SIRT1). Healthy male mice were assigned into normal and diabetic cataract groups. Blood glucose, lens turbidity, and apoptosis were measured. Lens epithelial cells were classified into the normal, blank, negative control (NC), mimics, inhibitors, siRNA-SIRT1, and inhibitors + siRNA-SIRT1 groups. , Bcl-2, Bax, p53, and SIRT1 expressions of each group were detected. Cell proliferation, cycle and apoptosis were tested by MTT assay and flow cytometry. can specifically bind to SIRT1 according to the luciferase system. SIRT1 protein concentration was strongly positive in normal mice and weakly positive in diabetic cataract mice. Apoptosis index of diabetic cataract mice was higher than the normal mice. Compared with normal mice, the expressions of , Bax, and p53 increased in diabetic cataract mice, while the Bcl-2 and SIRT1 expressions decreased. In comparison with the blank and NC groups, the expressions of , Bax, and p53 increased, while Bcl-2 and SIRT1 expressions decreased, and the proliferation decreased and apoptosis rate increased in the mimics and siRNA-SIRT1 groups; the results were contradicting for the inhibitor group. could promote apoptosis and inhibit proliferation of lens epithelial cells in diabetic cataract mice by targetting SIRT1.

摘要

我们的研究旨在通过靶向烟酰胺腺嘌呤二核苷酸(NAD)依赖性组蛋白去乙酰化酶沉默调节蛋白1(SIRT1),探讨其对糖尿病性白内障小鼠晶状体上皮细胞增殖和凋亡的影响。将健康雄性小鼠分为正常组和糖尿病性白内障组。检测血糖、晶状体混浊度和细胞凋亡情况。将晶状体上皮细胞分为正常组、空白组、阴性对照组(NC)、模拟物组、抑制剂组、小干扰RNA(siRNA)-SIRT1组以及抑制剂+siRNA-SIRT1组。检测每组中[未提及的物质]、Bcl-2、Bax、p53和SIRT1的表达。通过MTT法和流式细胞术检测细胞增殖、细胞周期和细胞凋亡情况。根据荧光素酶系统,[未提及的物质]可特异性结合SIRT1。SIRT1蛋白浓度在正常小鼠中呈强阳性,在糖尿病性白内障小鼠中呈弱阳性。糖尿病性白内障小鼠的凋亡指数高于正常小鼠。与正常小鼠相比,糖尿病性白内障小鼠中[未提及的物质]、Bax和p53的表达增加,而Bcl-2和SIRT1的表达降低。与空白组和NC组相比,模拟物组和siRNA-SIRT1组中[未提及的物质]、Bax和p53的表达增加,而Bcl-2和SIRT1的表达降低,细胞增殖减少,凋亡率增加;抑制剂组的结果则相反。[未提及的物质]可通过靶向SIRT1促进糖尿病性白内障小鼠晶状体上皮细胞的凋亡并抑制其增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e08/5529207/14316c5285ae/bsr-37-bsr20170695-g1.jpg

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