Luo Si, Li Shi, Zhu Lei, Fang Shu-Huan, Chen Jun-Li, Xu Qing-Qing, Li Hong-Ying, Luo Na-Chuan, Yang Cong, Luo Dan, Li Lin, Ma Xiao-Hui, Zhang Rong, Wang Hong, Chen Yun-Bo, Wang Qi
aInstitute of Clinical Pharmacology bGuangzhou University of Chinese Medicine, Guangzhou, China.
Neuroreport. 2017 Apr 12;28(6):299-306. doi: 10.1097/WNR.0000000000000749.
Baicalin, a plant-derived flavonoid, has been reported to exert neuroprotective effects on ischemia-like or excitotoxic injury. To confirm this function and explore the possible mechanism, we investigated the protective effect of baicalin on an in-vitro model of ischemia (oxygen-glucose deprivation-treated endothelial cell). In the present study, we found that baicalin (100 μM) inhibited cell death, reduced cell membrane damage, and maintained the integrity of the nucleus. Flow cytometric analysis and Hoechst 33258/propidium iodide double staining results showed that the necroptosis ratio decreased with baicalin treatment. Western blot analysis showed that baicalin regulated the expression of RIP-1 and RIP-3 in bEnd.3 cells and the use of detection kits showed that baicalin inhibited the production of reactive oxygen species and malondialdehyde, and increased the activity of superoxide dismutase in oxygen-glucose deprivation-treated bEnd.3 cells. These results indicated that baicalin effectively alleviated the oxidative stress, decreased the proportion of cells undergoing necrosis, and reduced cell damage.
黄芩苷是一种植物来源的黄酮类化合物，据报道其对缺血样或兴奋性毒性损伤具有神经保护作用。为证实这一功能并探索可能的机制，我们研究了黄芩苷对体外缺血模型（氧糖剥夺处理的内皮细胞）的保护作用。在本研究中，我们发现黄芩苷（100 μM）可抑制细胞死亡、减少细胞膜损伤并维持细胞核的完整性。流式细胞术分析以及Hoechst 33258/碘化丙啶双重染色结果显示，黄芩苷处理后坏死性凋亡比例降低。蛋白质免疫印迹分析表明，黄芩苷可调节bEnd.3细胞中RIP-1和RIP-3的表达，检测试剂盒检测结果显示，黄芩苷可抑制氧糖剥夺处理的bEnd.3细胞中活性氧和丙二醛的产生，并提高超氧化物歧化酶的活性。这些结果表明，黄芩苷可有效减轻氧化应激、降低坏死细胞比例并减少细胞损伤。
