Wei-hua Li, Chang-qing Sun, Qiang Xie, Rong Wu, Kai-min Lin
Department of Cardiology, The First Hospital of Xiamen, Fujian Medical University, The Cardiovascular Institute of Xiamen, China.
Arch Med Res. 2009 Feb;40(2):67-72. doi: 10.1016/j.arcmed.2008.12.006.
Group IIa secretory phospholipase A2 (sPLA2 IIa) induces atherosclerosis by altering systemic lipoprotein mechanism. The aim of this study was to investigate the expression and localization of sPLA2 IIa in atherosclerosis of rat aorta, myocardium and visceral adipose tissue (VAT) and to explore the effect of simvastatin on sPLA2 IIa expression.
Thirty male Wistar rats were randomly divided into three groups: control group, test group, and simvastatin group. Control group rats were fed with standard chow, whereas those in the test group were fed with a high cholesterol diet. Simvastatin (5 mg/kg/day per gavage) was given to the rats in simvastatin group in addition to the high cholesterol diet. At the end of 8 weeks, rats were sacrificed and sPLA2 IIa measured by immunocytochemistry.
sPLA2 IIa was present in smooth muscle cells, aortic plaques, and also in myocardium and VAT. In addition, sPLA2 IIa expression in myocardium and aorta was much higher in the test group than in control group (p <0.01). However, expression of the enzyme in myocardium and aorta was significantly decreased in the simvastatin group compared to the test group (p <0.05). Immunostaining of sPLA2 IIa was also present in VAT, but no significant changes were found in levels of this enzyme among the three groups (p >0.05).
Myocardium and VAT may be two other important sources of sPLA2 IIa. Our data support the hypothesis that sPLA2 IIa may play a significant role in the pathogenesis of atherosclerosis. Simvastatin may reduce the process of atherosclerosis by decreasing the expression level of sPLA2 IIa in myocardium and aorta.
IIa 型分泌性磷脂酶 A2（sPLA2 IIa）通过改变全身脂蛋白机制诱导动脉粥样硬化。本研究旨在探讨 sPLA2 IIa 在大鼠主动脉、心肌和内脏脂肪组织（VAT）动脉粥样硬化中的表达及定位，并探究辛伐他汀对 sPLA2 IIa 表达的影响。
将 30 只雄性 Wistar 大鼠随机分为三组：对照组、试验组和辛伐他汀组。对照组大鼠喂以标准饲料，而试验组大鼠喂以高胆固醇饮食。除高胆固醇饮食外，辛伐他汀组大鼠给予辛伐他汀（5mg/kg/天，经口灌胃）。8 周结束时，处死大鼠，通过免疫细胞化学法检测 sPLA2 IIa。
sPLA2 IIa 存在于平滑肌细胞、主动脉斑块中，也存在于心肌和 VAT 中。此外，试验组心肌和主动脉中 sPLA2 IIa 的表达远高于对照组（p<0.01）。然而，与试验组相比，辛伐他汀组心肌和主动脉中该酶的表达显著降低（p<0.05）。sPLA2 IIa 的免疫染色在 VAT 中也存在，但三组中该酶水平未发现显著变化（p>0.05）。
心肌和 VAT 可能是 sPLA2 IIa 的另外两个重要来源。我们的数据支持 sPLA2 IIa 可能在动脉粥样硬化发病机制中起重要作用这一假说。辛伐他汀可能通过降低心肌和主动脉中 sPLA2 IIa 的表达水平来减轻动脉粥样硬化进程。
