Atorvastatin inhibits cholesterol-induced caspase-3 cleavage through down-regulation of p38 and up-regulation of Bcl-2 in the rat carotid artery.

摘要: AIM Atherosclerotic lesions in the carotid arteries lead to a broad range of cerebrovascular disorders such as vascular dementia and ischaemic stroke. Recent studies have verified beneficial role atorvastatin (AV) atherosclerosis. Despite large body studies, mechanisms underlying this effect not been completely explained. In study, several experiments were performed on atherosclerotic rat models investigate anti-inflammatory anti-apoptotic AV artery. METHODS experimental 40 male Wistar rats (250 ± 25 g) randomly divided into four groups: normal diet (ND; n = 10); high-cholesterol (HD; plus (HD + AV; 10) ; control group (AV; 10). Cleavage caspase-3 protein, expression B-cell lymphoma 2 (Bcl-2) well phosphorylation p38 mitogen-activated protein kinase (MAPK) determined by immunoblotting assay artery homogenate. Plasma atherogenic indices, including total cholesterol (TC), high-density lipoprotein (HDL-C) low-density (LDL-C) measured colorimetric at end experiment. levels oxidised LDL (oxLDL) sandwich enzyme-linked immunosorbent (ELISA). RESULTS After eight weeks feeding with diet, an elevated level oxLDL was observed plasma HD compared ND [214.42 17.46 vs 69.13 9.92 mg/dl (5.55 0.45 1.78 0.26 mmol/l); p < 0.01]. administration significantly reduced [126.52 9.46 214.42 (3.28 0.25 5.55 Results also showed that HC group, had lower (p 0.05) higher Bcl-2 0.05). Lower cleaved comparison CONCLUSIONS The resultant data suggest could be partially mediated pro-inflammatory MAPK Atorvastatin can therefore considered target drug prevention or development events.