Wang Yan,Shi Xueqing,Qu Zhenyun,Wang Dongmei,Zhao Henan.Expression of COX-2 and mPGES-1 in rabbit coronary atherosclerotic tissues and effects of atorvastatin[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(07):643-646.
Wang Yan,Shi Xueqing,Qu Zhenyun,Wang Dongmei,Zhao Henan.Expression of COX-2 and mPGES-1 in rabbit coronary atherosclerotic tissues and effects of atorvastatin[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(07):643-646.DOI:
Expression of COX-2 and mPGES-1 in rabbit coronary atherosclerotic tissues and effects of atorvastatin
Objective To determine the expression of cyclooxygenase-2 (COX-2) and membrane associated prostaglandin E-1 (mPGES-1) in a rabbit model of atherosclerosis and determine the effects of ator-vastatin on the expression. Methods Forty male New Zealand rabbits (3 months old) were fed with normal diet (blank-control group
n=8) and high-cholesterol diet (n=32) respectively for 8 weeks. Then
the high-cholesterol diet rabbits were subsequently assigned to receive non-treatment (simple atherosclerotic model group)
and treatment groups with atorvastatin at 2.5
5 and 10 mg/(kg·d) respectively (n=8 for each group). Six weeks later
all rabbits were sacrificed and their coronaries were removed. The expression of COX-2 and mPGES-1
and serum levels of total cholesterol (TC)
triglyceride (TG)
high-density lipoprotein cholesterol (HDL-C),low-density lipoprotein cholesterol (LDL-C) and very low-density lipoprotein cholesterol (VLDL-C)were evaluated respectively. Results Compared with the blank-control group
the expression levels of COX-2 and mPGES-1
and the serum levels of total TC
TG
LDL-C and VLDL-C were all significantly increased
and HDL-C was significantly reduced in model group(P0.05). After being treated by atorvastatin with 5 mg/(kg·d) and 10 mg/(kg·d)
the levels of COX-2 and mPGES-1
and TC
TG
LDL and VLDL were significantly decreased
but HDL was increased compared with the corresponding values of the model rabbits (P0.05). Conclusion Atorvastatin may play anti-atherosclerotic inflammation role through down-regulating COX-2/mPGES-1 and reducing blood lipid.
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