Berberine is identified to lower the serum cholesterol level in human and hamster through the induction of low density lipoproteins (LDL) receptor in hepatic cells. To evaluate its potential in preventing atherosclerosis, the effect of berberine on atherosclerosis development in apolipoprotein E-deficient (apoE

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Although thiazolidinediones (TZDs) are potent promoters of adipogenesis in the preadipocyte, they induce apoptosis in several other cell types, such as cancer cells, endothelial cells and T‐lymphocytes. In this study, we investigated the proapoptotic effect of TZDs in mature 3T3‐L1 adipocytes, which express high levels of the peroxisome proliferator‐activated receptor‐γ (PPARγ) protein. Apoptosis was induced in mature 3T3‐L1 adipocytes by treatment with troglitazone, pioglitazone or prostaglandin J2, and could be blocked by the PPARγ antagonist GW9662. Treatment with PPARγ agonists also decreased Akt‐1 protein and phosphorylation levels without affecting phosphoinositide 3‐kinase and PTEN. Further analysis indicated that in troglitazone‐treated 3T3‐L1 adipocytes, Bad phosphorylation and Bcl‐2 protein levels were reduced, and Bax translocation to the mitochondria was increased. Subsequently, cytochrome c release and caspase‐3 cleavage were observed. TZD‐induced adipocyte apoptosis could be blocked by the caspase‐3 inhibitor Ac‐DEVD‐CHO or by overexpression of Bcl2. In cultured rat primary adipocytes, similar apoptosis‐inducing effects of troglitazone were also observed. Thus, TZDs promote apoptosis in adipocytes through a PPARγ‐dependent pathway. This apoptosis is mediated by the inhibition of Akt‐1, which decreases Bad phosphorylation and activates the mitochondrial apoptotic pathway.