高脂血症大鼠主动脉HSP22、TNF-α和eNOS的表达及阿托伐他汀的影响

Aortic expression of HSP22,TNF-α and eNOS in rats with hyperlipidemia and effects of atorvastatin

目的:研究高脂血症大鼠主动脉热休克蛋白22(HSP22)、肿瘤坏死因子α(TNF-α)及内皮型一氧化氮合酶(eNOS)的表达,以及阿托伐他汀对其的影响。方法:复制高脂血症大鼠模型后,实验分为正常对照组、高脂对照组和高脂+阿托伐他汀干预组。免疫组化法检测大鼠主动脉HSP22及TNF-α表达,Western blotting检测eNOS蛋白表达。结果:正常对照组未见HSP22和TNF-α阳性表达;高脂对照组与他汀干预组可见HSP22和TNF-α阳性表达;他汀干预组HSP22和TNF-α平均吸光度值明显低于高脂对照组(0.211±0.014 vs 0.345±0.042,0.218±0.090 vs 0.377±0.094,均P<0.05)。高脂对照组和他汀干预组eNOS表达均较正常对照组明显降低(P<0.01),高脂对照组和他汀干预组差异无显著。结论:HSP22和TNF-α在高脂血症大鼠主动脉中的表达升高,而eNOS的表达降低,阿托伐他汀的干预可降低HSP22和TNF-α的表达,但未能改变eNOS的表达。

AIM： To establish a rat hyperlipidemia model for studying the aortic expression of heat shock protein22（ HSP22）,tumor necrosis factor alpha（ TNF-α） and endothelial nitric oxide synthase（ eNOS） and the effect of atorvastatin intervention. METHODS： Hyperlipidemia model was established in SD rats. Afterwards,the rats were divided into normal control group,high fat group and high fat ＋ atorvastatin intervention group. The expression of HSP22 and TNF-α in the rat aortas was detected by immunohistochemical assay and the expression of eNOS was assessed by Western blotting. RESULTS： No detectable expression of HSP22 and TNF-α in the normal control group was observed. However,the expression of HSP22 and TNF-α was positive in the high fat group and the atorvastatin intervention group. The mean densities of HSP22 and TNF-α positive particles were significant lower in the atorvastatin intervention group as compared with high fat group（ both P 〈0.05）. The expression of eNOS protein in the high fat group and atorvastatin intervention group was significantly lower than that in normal control group（ P 〈0. 01）. However,no marked difference of eNOS protein expression between high fat group and atorvastatins intervention group was observed. CONCLUSION： The expression of HSP22 and TNF-α in the rat aortas is increased in the hyperlipidemia rat model. This effect can be restored by atorvastatin treatment. The expression of eNOS in the rat aortas is decreased in the hyperlipidemia rat model,but this tendency could not be attenuated by atorvastatin.