Curcumin ameliorates ischemic stroke injury by downregulating GMFB expression: An in vitro study

• الحاوية / القاعدة: Biomolecules & Biomedicine
• المؤلفون الرئيسيون: Xiumei Bai, Yabin Song, Xiangyan Zhang, Liqiong Liu, Haixia Wu, Jiaqing Feng, Lihong Wu, Huizhen Liu, Diangui Zhou
• التنسيق: مقال
• اللغة: الإنجليزية
• منشور في: Association of Basic Medical Sciences of Federation of Bosnia and Herzegovina 2024-09-01
• الموضوعات: Ischemic stroke; curcumin; GMFB; BMECs; OGD/R
• الوصول للمادة أونلاين: https://www.bjbms.org/ojs/index.php/bjbms/article/view/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.