Bai Xiumei, Song Yabin, Zhang Xiangyan, Liu Liqiong, Wu Haixia, Feng Jiaqing, Wu Lihong, Liu Huizhen, Zhou Diangui
Pharmaceutical Department, Zhongshan Torch Development Zone People's Hospital, Zhongshan, China.
Department of Neurology, Xiangan Hospital Affiliated to Xiamen University Xiamen, Fujian, China.
Biomol Biomed. 2025 Jan 30;25(3):578-587. doi: 10.17305/bb.2024.10957.
Ischemic stroke (IS) is a cerebrovascular sickness, and cerebral ischemia-reperfusion (I/R) damage often occurs, but there is still a lack of drugs that can significantly alleviate it. Curcumin (Cur) exerts pharmacological effects such as antioxidative stress, anti-inflammation, and the promotion of apoptosis through regulating various pathways, but its efficacy and specific mechanism of action in IS have not been fully clarified. The purpose of this paper is to study the influence of Cur on IS. Brain microvascular endothelial cells (BMECs) were used to create an oxygen-glucose deprivation/reoxygenation (OGD/R) model to simulate I/R damage. The cell viability was assessed using an MTT assay. The LDH level and ROS positive rate were measured using commercial kits. The cell invasion was examined using a transwell assay. The apoptosis was assessed by flow cytometry. The contents of GMFB, Bax, and Bcl2 were measured using western blot. We confirmed that in the OGD/R-induced IS cell model, the abundance of GMFB was enhanced in the OGD/R group versus the control group. GMFB overexpression promoted OGD/R-induced cell viability diminution, increased LDH and ROS levels, lessened cell invasion ability, enhanced cell apoptosis, enhanced Bax levels, and decreased Bcl2 levels. Silencing GMFB ameliorated OGD/R-induced cell damage. Cur ameliorated OGD/R-induced cell damage. Cur curbed OGD/R-induced cell damage by downregulating GMFB expression. In conclusion, Cur cured ischemic stroke-induced cell damage by downregulating GMFB expression.
缺血性中风（IS）是一种脑血管疾病，常发生脑缺血再灌注（I/R）损伤，但仍缺乏能显著缓解该损伤的药物。姜黄素（Cur）通过调节多种途径发挥抗氧化应激、抗炎和促进细胞凋亡等药理作用，但其在IS中的疗效和具体作用机制尚未完全阐明。本文旨在研究Cur对IS的影响。利用脑微血管内皮细胞（BMECs）建立氧糖剥夺/复氧（OGD/R）模型以模拟I/R损伤。采用MTT法评估细胞活力。使用商业试剂盒测定乳酸脱氢酶（LDH）水平和活性氧（ROS）阳性率。采用Transwell法检测细胞侵袭能力。通过流式细胞术评估细胞凋亡。使用蛋白质免疫印迹法测定生长停滞特异性蛋白6（GMFB）、促凋亡蛋白Bax和抗凋亡蛋白Bcl2的含量。我们证实，在OGD/R诱导的IS细胞模型中，与对照组相比，OGD/R组中GMFB的丰度增加。GMFB过表达促进了OGD/R诱导的细胞活力降低，增加了LDH和ROS水平，降低了细胞侵袭能力，增强了细胞凋亡，提高了Bax水平，并降低了Bcl2水平。沉默GMFB可改善OGD/R诱导的细胞损伤。Cur可改善OGD/R诱导的细胞损伤。Cur通过下调GMFB表达抑制OGD/R诱导的细胞损伤。总之，Cur通过下调GMFB表达治愈缺血性中风诱导的细胞损伤。
