Eye Institute, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Department of Ophthalmology, People's Hospital of Jiangyin, Wuxi, Jiangsu, China.
Curr Eye Res. 2021 Aug;46(8):1159-1165. doi: 10.1080/02713683.2020.1869266. Epub 2021 Jan 18.
Exposure of 0.2 mM HO in lenses resulted in obvious cloudiness and typical pathological changes of cataract such as rupture of the lens capsule, degenerative lens epithelial cells (LECs), etc. Rg1 effectively prevented lens opacity caused by HO. After Rg1 treatment, lens WSP content, the level of SOD, total GSH, and reduced GSH were increased, while the level of MDA and oxidized GSH were decreased. In addition, MDA concentration of lens by Rg1 treatment only was found to be lower than the controls. Rg1 attenuated HO-induced cell injury at the concentration of 0.4 mM that it elevated cell activity, and peaked at 0.6 mM.
This study demonstrated that Rg1 might have the capability to protect lens against oxidative stress-induced cataract, at least by local administration. LECs: lens epithelial cells; Rg1: Ginsenoside Rg1; SD: Sprague-Dawley; ROS: reactive oxygen species; SOD: Superoxide Dismutase; GSH: glutathione; MDA: Malonediadehyde; HO Hydrogen peroxide.
在晶状体中暴露于 0.2 mM 的 HO 导致明显的混浊和白内障的典型病理变化,如晶状体囊破裂、变性的晶状体上皮细胞(LEC)等。Rg1 能有效防止 HO 引起的晶状体混浊。Rg1 处理后,晶状体 WSP 含量、SOD 水平、总 GSH 和还原型 GSH 增加,而 MDA 和氧化型 GSH 的水平降低。此外,Rg1 处理的晶状体 MDA 浓度低于对照组。Rg1 在 0.4 mM 的浓度下减弱了 HO 诱导的细胞损伤,提高了细胞活性,在 0.6 mM 时达到峰值。
本研究表明,Rg1 至少通过局部给药具有保护晶状体免受氧化应激诱导的白内障的能力。LEC:晶状体上皮细胞;Rg1:人参皂苷 Rg1;SD:Sprague-Dawley;ROS:活性氧;SOD:超氧化物歧化酶;GSH:谷胱甘肽;MDA:丙二醛;HO:过氧化氢。