林惠军,杨倩,龚潇.野黄芩素经Akt/FoxO1信号通路抑制视网膜神经节细胞凋亡.[J].中南医学科学杂志.,2022,(4):482-485, 490.
野黄芩素经Akt/FoxO1信号通路抑制视网膜神经节细胞凋亡
The mechanism of scutellariae inhibiting apoptosis of retinal ganglion cells via Akt/FoxO1 signaling pathway
投稿时间:2021-04-26  修订日期:2021-09-12
DOI:10.15972/j.cnki.43-1509/r.2022.04.004
中文关键词:  野黄芩素  Akt/FoxO1信号通路  视网膜神经节细胞  细胞凋亡
英文关键词:scutellarin  Akt/FoxO1 signaling pathway  retinal ganglion cell  apoptosis
基金项目:四川省卫生和计划生育委员会科研课题(18PJ090) 作者简介:林惠军,副主任医师,研究方向为白内障、视网膜疾病的诊治,E-mail为1013228336@qq.com。
作者单位E-mail
林惠军 四川大学华西医院龙泉医院眼科,四川省成都市610100 e-mail为1013228336@qq.com 
杨倩 四川大学华西医院龙泉医院眼科,四川省成都市610100  
龚潇 四川大学华西医院龙泉医院眼科,四川省成都市610100  
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中文摘要:
      目的探讨野黄芩素经Akt/叉头状转录因子O1(FoxO1)信号通路抑制视网膜神经节细胞(RGC)凋亡的机制。方法构建视网膜神经RGC-5细胞氧化应激损伤模型,野黄芩素组分别给与25和100 μmol/L野黄芩素,阳性对照组给予25 μmol/L拉坦前列素,设模型组和阴性对照组。检测各组细胞增殖和凋亡情况,以及RGC-5细胞活性氧(ROS)、超氧化物歧化酶(SOD)及凋亡相关蛋白的水平。结果与阴性对照组比较,其他组细胞增殖率、SOD、p-Akt/Akt、p-FoxO1/FoxO1和B细胞淋巴瘤/白血病-2(Bcl-2)水平降低,细胞凋亡率、ROS、Bcl-2相关X蛋白(Bax)和Caspase-3水平增加(P<0.05)。与模型组比较,野黄芩素组和阳性对照组细胞增殖率、SOD、p-Akt/Akt、p-FoxO1/FoxO1和Bcl-2水平增加,细胞凋亡率、ROS、Bax和Caspase-3水平降低;且随野黄芩素剂量增加差异更为显著,但阳性对照组作用最明显(P<0.05)。结论野黄芩素可以抑制RGC-5细胞凋亡,其机制可能与激活Akt/FoxO1信号通路有关。
英文摘要:
      To investigate the mechanism of scutellarin inhibiting retinal ganglion cell (RGC) apoptosis through protein kinase B (Akt)/forkhead transcription factor O1 (FoxO1) signal pathway. MethodsThe oxidative stress injury model of retinal nerve RGC-5 cells was established and given 25 and 100 μmol/L scutellarin respectively, the positive control group was given 25 μmol/L latanoprost, and model group and negative control group were set up. The proliferation and apoptosis of cells in each group, as well as the levels of reactive oxygen species (ROS), superoxide dismutase (SOD) and apoptosis related proteins in RGC-5 cells were detected. ResultsCompared with the negative control group, the cell proliferation rate, SOD, p-Akt/Akt, p-FoxO1/FoxO1 and B-cell lymphoma/leukemia-2 (Bcl-2) levels in other groups decreased, and the apoptosis rate, ROS, Bcl-2 related X protein (Bax) and Caspase-3 levels increased(P<0.05). Compared with the model group, the cell proliferation rate, SOD, p-Akt/Akt, p-FoxO1/FoxO1 and Bcl-2 levels in the scutellarin group and the positive control group increased, while the apoptosis rate, ROS, Bax and Caspase-3 levels decreased; The difference was more significant with the increase of the dose of scutellarin, but the effect of the positive control group was the most obvious(P<0.05). ConclusionScutellarin can inhibit RGC-5 cell apoptosis, and its mechanism may be related to the activation of Akt/FoxO1 signal pathway.
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