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Ursolic acid suppresses IL-6 induced C-reactive protein expression in HepG2 and protects HUVECs from injury induced by CRP. | LitMetric

Ursolic acid suppresses IL-6 induced C-reactive protein expression in HepG2 and protects HUVECs from injury induced by CRP.

Eur J Pharm Sci

Department of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, 9 West Section, Lvshun South Road, Dalian 116044, Liaoning Province, China.

Published: January 2012

Objective: To investigate the inhibitory effects of ursolic acid (UA) on the expression of C-reactive protein (CRP) induced by IL-6 in HepG2 cells and the protective effects on the CRP-induced injury to human umbilical vein endothelial cells (HUVECs).

Methods: HepG2 cells were treated with IL-6 or IL-6 and different concentrations of UA for 48 h, then the cells were collected. The total protein and RNA of the cells were extracted for western blotting and RT-PCR methods to detect CRP protein and mRNA expression. HUVECs were treated with CRP or CRP and different concentrations of UA for 24h. Cell proliferation in each group was assayed by MTT. Cells were collected for western blotting and RT-PCR methods to detect VCAM-1, LOX-1 protein or mRNA expression.

Result: IL-6 can significantly increase CRP protein and mRNA expression in HepG2 cells, and this effect of IL-6 can be decreased by UA (6.25, 12.5, 25 μmol/L) markedly in a dose-dependent manner. UA can inhibit CRP-induced proliferation of HUVECs. CRP can obviously increase LOX-1/VCAM-1 expression in HUVECs, both on mRNA and protein levels and the effect of CRP can be inhibited by UA (5, 10, 20 μmol/L) in a dose-dependent manner.

Conclusion: UA can reduce the over expression of CRP in HepG2 cells induced by IL-6 and inhibit the increased expression of VCAM-1 and LOX-1 in HUVECs caused by CRP. Our research suggests that UA can reduce CRP levels in plasma and prevent inflammatory cytokines from injuring endothelial cells by inhibiting the hepatic synthesis of CRP. So UA may have positive significance for prevention and treatment of atherosclerosis and other cardiovascular diseases.

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http://dx.doi.org/10.1016/j.ejps.2011.11.002DOI Listing

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