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Abstract

Protective Effect of Curcumin on Lipopolysaccharide-Induced Rat Cardiomyocyte Hypertrophy

Author(s): Yuanzhou Lu, Wei Gong, Xin Yi* and Xiaohui Lu
Department of Cardiology, Medical School, Affiliated Tongzhou Hospital of Nantong University, Nantong University, Nantong, Jiangsu 226399, 1Department of Human Anatomy, Medical School, Nantong University, 2Department of Stomatology, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, China

Correspondence Address:
Xin Yi, Department of Human Anatomy, Medical School, Nantong University, Nantong, Jiangsu 226001, China, E-mail: [email protected]


To study the protective effect of curcumin on lipopolysaccharide-induced rat cardiomyocyte hypertrophy is the main objective of the study. Cardiomyocytes were purified and cultured by differential adherence in in vitro and then they were divided into control group, lipopolysaccharide group, lipopolysaccharide+curcumin low-dose (12.5 mg/l) group, lipopolysaccharide+curcumin medium-dose (25 mg/l) group and lipopolysaccharide+curcumin high-dose (50 mg/l) group. The morphological changes were observed under a phase-contrast inverted microscope and the cell volume was measured. The total protein content of the cell was detected by Coomassie brilliant blue kit. Enzyme-linked immunosorbent assay method was used to detect the level of tumor necrosis factor alpha. The TILL imaging system was used to observe the changes in intracellular calcium ions. Compared with the control group, lipopolysaccharide significantly increased the cardiomyocyte volume, the total cell protein content, the level of tumor necrosis factor alpha (p<0.01) and the instantaneous peak of calcium ions. Compared with the lipopolysaccharide group, 12.5, 25, 50 mg/l curcumin treatment inhibited the increase of cardiomyocyte volume, total protein content, tumor necrosis factor alpha level and the instantaneous peak of calcium ions induced by lipopolysaccharide and showed a dose-dependent effect. Curcumin has a protective effect on rat cardiomyocyte hypertrophy induced by lipopolysaccharides, which may be related to the inhibition of tumor necrosis factor alpha production and the inhibition of calcium ions overload.

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