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WANG Yan, ZANG Pei, LIANG Ling-jun.et al, . Inhibitive effects of ginsenoside Rg1 on cardiomyocyte hypertrophy induced by tumor necrosis factor-[J]. Chinese Journal of Public Health, 2014, 30(1): 77-79. DOI: 10.11847/zgggws2014-30-01-23
Citation: WANG Yan, ZANG Pei, LIANG Ling-jun.et al, . Inhibitive effects of ginsenoside Rg1 on cardiomyocyte hypertrophy induced by tumor necrosis factor-[J]. Chinese Journal of Public Health, 2014, 30(1): 77-79. DOI: 10.11847/zgggws2014-30-01-23

Inhibitive effects of ginsenoside Rg1 on cardiomyocyte hypertrophy induced by tumor necrosis factor-

  • Objective To investigate protective effects and mechanism of ginsenoside Rg1 on cardiomyocyte hypertrohy induced by tumor necrosis factor-α(TNF-α) in neonatal rats.Methods The primary cultured of neonatal rat ventricular myocytes were used and the hypertrophic cardiac myocytes were induced by TNF-α at the dose of 100 μg/L,and then the effect of different concentrations of ginsenoside Rg1 on cardiac hypertrophy was observed.Total protein content was assayed with Lowery method;the expressions of atrial natriuretic peptide (ANP)and Toll like receptor 4(TLR4)mRNA were determined with reverse transcription-polymerase chain reaction(RT-PCR);the expression of TLR4 and inhibitor-κBα (IκBα)was measured by western blot.Results Compared with those of the control group,protein content,ANP mRNA,and TLR4 mRNA and protein were significantly increased(P<0.01 for all)and IκBα decreased in TNF-α group (P<0.01).Compared with TNF-α group,ginsenoside Rg1 of 30 μmol/L significantly inhibited TNF-α-induced cardiac hypertrophy and decreased the protein content (19.76±1.09 μg)(P<0.05)and the expression of ANP mRNA(0.609±0.001)(P<0.05).Ginsenoside Rg1 at dose of 30 μmol/L could also significantly alleviate the inflammatory response induced by TNF-α,which may be partially via attenuating IκBα(0.70±0.09)(P<0.05)and the high expression of TLR4 mRNA (0.899±0.001)and protein(0.46±0.03)induced by TNF-α.Conclusion Ginsenoside Rg1 has protective effect on TNF-α-induced cardiac hypertrophy.The mechanism may be related to the inhibition of TLR4/NF-κB.
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