The Effects of Atorvastatin on Protein Kinase C and C-reactive Protein in Experimental Atherosclerosis

Objective To reveal the protective effects of atorvastatin against atherosclerosis independent of cholesterol-lowering effect, we investigated the effects of atorvastation on the expression of protein kinase C (PKC) and C-reactive protein in experimental atherosclerosis of rats. Method Fifty female Sprague-Dawley rats were randomly divided into normal diet group (n=10, control group), vitamin D3 injection and high cholesterol diet group (n=40). After 8 weeks, vitamin D3 injection and high cholesterol diet rats were randomized to receive either atorvastatin (5 mg•kg^(-1)•d^(-1)) (n=20, atorvastatin group) or normal diet (n=20, model group). Another eight weeks later, all rats were killed and part of their aortas were examined by light and electron microscope and the left were removed for western blot analysis to measure PKC; At the begin and end of experiment, serumcollected for lipid and C-reactive protein determining determination. Results Cholesterol, low-density lipoprotein, triglyceride levels in atorvastatin group were significantly lower than those in model group but higher than control group. The pathologic changes in atorvastatin group were less severe than those in model group, there showed no any pathological changes in control group. The levels of C-reactive protein in model group [(18.64±0.94) mg/L] were higher than those in control group [(9.21±0.21) mg/L] (P＜0.05). C-reactive protein levels also differed significantly between control and atorvastatin group (12.52±0.65 mg/L) (P＜0.05). PKC levels were significantly higher in model group (7786.12 ± 264.75) and atorvastatin group (4267.57 ± 233.94) than in control group (2468.75 ± 145.53)(all P＜0.05). But compared with model group, PKC levels were markedly lower in the atorvastatin group (P＜0.01). Conclusions Atorvastatin may be useful not only as a cholesterol-lowering agents but also as anti-arteriosclerotic agent that provide vascular protection by inhibition PKC expression and inflammatory reaction.