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The effects of atorvastatin on group Ⅱ a secretory phospholipaseA2 and nuclear factor-kappaB expression in atherosclerosis rats

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Author:
LI Wei-hua(Department of Cardiology, Xiamen First Hospital Affiliated to Fujian Medical University. Xiamen 361003, China)
SUN Chang-qing(Department of Cardiology, Xiamen First Hospital Affiliated to Fujian Medical University. Xiamen 361003, China)
XIE Qiang(Department of Cardiology, Xiamen First Hospital Affiliated to Fujian Medical University. Xiamen 361003, China)
WU Rong(Department of Cardiology, Xiamen First Hospital Affiliated to Fujian Medical University. Xiamen 361003, China)
CHEN Pei-4qiong(Department of Cardiology, Xiamen First Hospital Affiliated to Fujian Medical University. Xiamen 361003, China)
ZHANG Hai-ping(Department of Cardiology, Xiamen First Hospital Affiliated to Fujian Medical University. Xiamen 361003, China)
Journal Title:
CHINA MEDICINE
Issue:
Volume 5, Issue 03, 2010
DOI:
10.3760/cma.j.issn.1673-4777.2010.03.002
Key Word:
Atherosclerosis; Group Ⅱa secretory phospholipase A2; Nuclear factor-kappaB; Atorvastatin

Abstract: Objective To observe the effects of atorvastatin on nuclear factor-kappaB (NF-κB) and group Ⅱ a secretory phospholipaseA2 (sPLA2 Ⅱ a) expression in aorta of atherosclerosis(AS) rat. Methods Healthy male Wistar rats were randomly divided into 3 groups(10 rats in each group) :control group, model group(40 mg/(kg·d) per gavage). The rats in model group and atorvastatin group were fed with high cholesterol group and atorvastatin diet. At the end of 8 weeks, the expression of sPLA2 Ⅱ a and NF-κB were observed by immunocytochemistry and re-verse transcription polymerase chain reaction (RT-PCR). Results The expression of NF-κB and the gene expres-sion of sPLA2 Ⅱ a and mRNA levels of the model group significantly increased compared with those in the control group(all P <0.01) and could be significantly attenuated by atorvastatin. The expression of sPLA2-Ⅱ a mRNA was correlated with NF-κB in all groups. Conclusions sPLA2-Ⅱ a may play a significant role in the pathogenesis of AS. Atorvastatin can relieve the process of AS by decreasing the expression level of sPLA2-Ⅱa. NF-κB may stimu-late the gene transcription of sPLA2-Ⅱa.

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