Liv.52 regulates ethanol induced PPARγ and TNF α expression in HepG2 cells
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- Mitra, S.K., Varma, S.R., Godavarthi, A. et al. Mol Cell Biochem (2008) 315: 9. doi:10.1007/s11010-008-9782-9
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Liver is a prime target of alcohol-induced damage by inducing inflammatory cytokines especially tumor necrosis factor alpha (TNFα). Activator of peroxisome proliferator activator receptor gamma (PPARγ) is protective against alcohol-induced liver injury in animals. Liv.52, one of the major herbal hepatoprotective drugs, is shown to protect the liver from toxicity and is considered to be an effective hepatoprotective agent. However, the signal pathway involved in the Liv.52-induced hepatoprotection is not understood well especially in the case of cultured liver cells treated with ethanol. Hence, the study was aimed at determining whether ethanol and Liv.52 could modulate PPARγ and TNFα induction in human hepatoma cells, HepG2. The present study with RT-PCR and confocal microscopy experiments showed that ethanol (100 mM) induced suppression of PPARγ expression in HepG2 cells. The ethanol-induced PPARγ suppression was abrogated by Liv.52. Moreover, Liv.52 also induced upregulation of PPARγ mRNA in liver cells as compared to the untreated cells. Further, 100 mM ethanol has also induced TNFα gene expression in HepG2 cells and interestingly Liv.52 abolished ethanol-induced TNFα. The study also shows that Liv.52 alone downregulated TNFα expression in HepG2 cells. Taken together, these findings suggest that Liv.52 is capable of attenuating ethanol-induced expression of TNFα and abrogating ethanol-induced suppression of PPARγ in liver cells. These results indicate that Liv.52-induced PPARγ expression and concomitant suppression of ethanol-induced elevation of TNFα in HepG2 cells suggest the immunomodulatory and hepatoprotective nature of Liv.52.