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Effects of tanshinone IIA on the hepatotoxicity and gene expression involved in alcoholic liver disease

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Abstract

Tanshinone IIA is one of the most abundant constituents of the root of Salvia miltiorrhiza BUNGE which exerts antioxidant and anti-inflammatory actions in many experimental disease models. In the present study, we demonstrated that the standardized fraction of S. miltiorrhiza (Sm-SF) was able to protect RAW 264.7 cells from ethanol-and lipopolysaccharide (LPS)-induced production of superoxide radical, activation of NADPH oxidase and subsequently death of the cells. Among four main components of Sm-SF, tanshinone IIA was the most potent in protecting cells from LPS-and ethanol-induced cytotoxicity. LPS or ethanol induced the expression of CD14, iNOS, and SCD1 and decreased RXR-α, which was completely reversed by tanshinone IIA. In H4IIEC3 cells, 10 μM tanshinone IIA effectively blocked ethanol-induced fat accumulation as evidenced by Nile Red binding assay. These results indicate that tanshinone IIA may have potential to inhibit alcoholic liver disease by reducing LPS-and ethanol-induced Kupffer cell sensitization, inhibiting synthesis of reactive oxygen/nitrogen species, inhibiting fatty acid synthesis and stimulating fatty acid oxidation.

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Correspondence to Byung-Hoon Lee.

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Yin, HQ., Kim, YS., Choi, YJ. et al. Effects of tanshinone IIA on the hepatotoxicity and gene expression involved in alcoholic liver disease. Arch. Pharm. Res. 31, 659–665 (2008). https://doi.org/10.1007/s12272-001-1209-2

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  • DOI: https://doi.org/10.1007/s12272-001-1209-2

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