Aloe-Emodin Protects RIN-5F (Pancreatic β-cell) Cell from Glucotoxicity via Regulation of Pro-Inflammatory Cytokine and Downregulation of Bax and Caspase 3

被引:34
作者
Alshatwi, Ali A. [1 ]
Subash-Babu, P. [1 ]
机构
[1] King Saud Univ, Adipogenesis & Immunobiol Res Lab, Dept Food Sci & Nutr, Coll Food Sci & Agr, Riyadh 11451, Saudi Arabia
关键词
Aloe-emodin; Glucotoxicity; RIN-5F cells; Apoptosis; ROS; INHIBITS ADIPOCYTE DIFFERENTIATION; OXIDATIVE STRESS; APOPTOSIS; GLUCOSE; ISLETS; PROLIFERATION; TOXICITY; RECEPTOR; DEATH; ASSAY;
D O I
10.4062/biomolther.2015.056
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
To determine the protective effect of aloe-emodin (AE) from high glucose induced toxicity in RIN-5F (pancreatic beta-cell) cell and restoration of its function was analyzed. RIN-5F cells have been cultured in high glucose (25 mM glucose) condition, with and without AE treatment. RIN-5F cells cultured in high glucose decreased cell viability and increased ROS levels after 48 hr compared with standard medium (5.5 mM glucose). Glucotoxicity was confirmed by significantly increased ROS production, increased pro-inflammatory (IFN-gamma, IL-1 beta,) & decreased anti-inflammatory (IL-6&IL-10) cytokine levels, increased DNA fragmentation. In addition, we found increased Bax, caspase 3, Fadd, and Fas and significantly reduced Bcl-2 expression after 48 hr. RIN-5F treated with both high glucose and AE (20 mu M) decreased ROS generation and prevent RIN-5F cell from glucotoxicity. In addition, AE treated cells cultured in high glucose were transferred to standard medium, normal responsiveness to glucose was restored within 8hr and normal basal insulin release within 24 hr was achieved when compared to high glucose.
引用
收藏
页码:49 / 56
页数:8
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