Suppressive effects of berberine on atherosclerosis via downregulating visfatin expression and attenuating visfatin-induced endothelial dysfunction

Abstract

Berberine (BBR) possesses significant anti-Atherosclerosis properties. Visfatin is one of the most promising biomarkers of incoming atherosclerosis. However, research on the effect of BBR on regulating visfatin expression in atherogenesis remains largely unknown. In this study, we investigated the effects of BBR on visfatin expression and atherogenesis in apolipoprotein E knockout (ApoE-/-) mice. The effect of BBR on attenuating visfatin-induced endothelial dysfunction was also evaluated in cultured human umbilical vein endothelial cells (HUVECs). In vivo experiments showed that BBR treatment (5 mg/kg/day) significantly reduced the serum levels of visfatin, lipid, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), the protein expression of visfatin, p-p38 MAPK and p-c-Jun N-Terminal kinase (JNK) in mice aorta and the distribution of visfatin in the atherosclerotic lesions in ApoE-/-m ice fed w ith a Western d iet. I n a ddition, in vitro experiments indicated that visfatin (100 μg/l) significantly increased apoptosis, the contents of IL-6 and TNF-α, the protein levels of p-p38 MAPK, p-JNK and Bax in HUVECs, which were reversed by BBR administration (50 μmol/l). Our findings suggest that BBR significantly ameliorates Western diet-induced atherosclerosis in ApoE-/-mice via downregulating visfatin expression, which is related to the inhibition of p38 MAPK and JNK signaling pathways and subsequent suppression of visfatin-induced endothelial dysfunction.