Inhibitory Action And Mechanism Of Ginsenoside Rg1on Cardiomyocyte Hypertrophy Induced By Tumor Necrosis Factor-α

ObjectiveTo investigate protective effects of Ginsenoside Rg1on cardiomyocytehypertrophy induced by tumor necrosis factor-α (TNF-α), and to explore itsmolecular mechanism.MethodsThe primary cultured of neonatal rat ventricular myocytes were as models,the hypertrophic cardiac myocytes were induced by TNF-α of100μg/L, andthe effect of different concentrations of Ginsenoside Rg1on cardiachypertrophy was observed. In order to observe the effect of NF-B and TLR4in TNF-α-induced hypertrophic cardiac myocytes, we used NF-B inhibitorBAY11-7082. Myocytes were randomly divided into6groups: Control,BAY11-7082, TNF-α, TNF-α+BAY11-7082, TNF-α+Ginsenoside Rg115μmol/L, TNF-α+Ginsenoside Rg130μmol/L. Total protein content wasassayed by the method of Lowery method; the cell size was measured bycomputer photograph analysis system; the expression of atrial natriureticpeptide (ANP) and Toll like receptor4(TLR4) mRNA were determined byReverse Transcription-Polymerase Chain Reaction(RT-PCR); the expressionof TLR4and inhibitor-κBα (IκBα) were measured by Western blot. ResultsCompared with control group, protein content, cell size, ANP mRNA,TLR4mRNA and TLR4protein were significantly increase (P<0.01), and IκBαdecrease (P<0.01) in TNF-α group. Compared with TNF-α group, GinsenosideRg1groups were significantly able to inhibit the TNF-α-induced cardiachypertrophy, expressed as the protein content (P<0.01), cell size and theexpression of ANP mRNA (P<0.01) decreased; Ginsenoside Rg1groups canalso significantly abolish the inflammatory response induced by TNF-α, whichis partially via attenuating IκBα (P<0.01) and the high expression of TLR4mRNA and protein induced by TNF-αConclusionGinsenoside Rg1has a protective effect on TNF-α-induced cardiachypertrophy, the mechanism may be related to the inhibition of TLR4/NF-Bsignal pathway.