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Aims/Introduction  An elevated level of plasma homocysteine has long been suspected as a metabolic risk factor for the development of atherosclerotic vascular diseases in diabetes. Berberine ( BBR ) has several preventive effects on cardiovascular diseases. The effects of  BBR  on atherosclerotic plaque stability increased by homocysteine thiolactone ( HTL ) remain unknown.    Materials and Methods  The model of atherosclerotic vulnerable plaque was induced by placing a collar around the carotid artery in  Apoe   −/−   mice. Endothelium‐dependent relaxation was assayed by organ chamber.    Results  Homocysteine thiolactone (50 mg/kg/day, 8 weeks) reduced the atherosclerotic plaque stability in the carotid artery of  Apoe   −/−   mice, which was reversed by  BBR  administration (1.0 g/kg/day).  In vivo  and  ex vivo  experiments showed that  HTL  dramatically reduced acetylcholine‐induced endothelium‐dependent relaxation and superoxide dismutase activity, and increased malondialdehyde content, which were inhibited by  BBR . Importantly, all effects induced by  BBR  were abolished by  GW 9662, an antagonist of peroxisome proliferator‐activated receptor‐γ. Incubation of cultured endothelial cells with  HTL  significantly reduced cell viabilities and enhanced production of reactive oxygen species. Pretreatment of cells with  BBR  dose‐dependently reversed  HTL ‐induced detrimental effects, which were  GW 9662‐reversible.    Conclusions  Berberine increases atherosclerotic plaque stability in hyperhomocysteinemia mice, which is related to the activation of peroxisome proliferator‐activated receptor‐γ and subsequent suppression of oxidative stress in endothelial cells.

journal of diabetes investigation

Berberine activates peroxisome proliferator‐activated receptor gamma to increase atherosclerotic plaque stability in  Apoe   −/−   mice with hyperhomocysteinemia