二十二碳六烯酸对肺动脉高压大鼠活化T细胞核因子c1表达的影响

Effect of Docosahexaenoic Acid on the Expression of NFATc1 in Pulmonary Hypertension Rats

目的观察二十二碳六烯酸(DHA)对野百合碱(MCT)致肺动脉高压(PH)大鼠肺血管重构及活化T细胞核因子c1(NFATc1)表达的影响。方法 24只SD大鼠随机分为正常对照组(n=7)、DHA干预组(n=7)及MCT模型组(n=10)。肺动脉高压模型采用MCT诱导法,HE染色观察大鼠肺小动脉形态学改变,免疫组织化学、Western blot和qRT-PCR检测大鼠肺动脉NFATc1蛋白和mRNA的表达。结果 DHA能明显减轻模型大鼠的肺血管重构;与正常对照组相比,MCT模型组肺动脉NFATc1蛋白和mRNA的表达明显增强(P<0.05);与MCT模型组相比,DHA干预组肺动脉NFATc1蛋白和mRNA的表达减弱(P<0.05)。结论 DHA对MCT所致肺动脉高压具有较好的抑制作用,其作用机制可能与其抑制NFATc1表达有关。

Aim To investigate the effects of docosahexaenoic acid（ DHA） on monocrotaline-induced pulmonary hypertension（ PH） in rats,and explore the potential mechanism involved in its action. Methods 24 male SpragueDawley rats were randomly divided into three groups： nomal control group（ n = 7）,DHA-treated group（ n = 7） and pulmonary hypertension model group（ n = 10）. The monocrotaline（ MCT）-induced pulmonary arterial hypertention was established.The microcosmic changes of pulmonary arterial morphologic in lung of rats were measured by optical microscope after the stain of HE. The expression of NFATc1 protein and mRNA levels in pulmonary arterial were detected by immunohistochemistry,Western blot,and qRT-PCR,respectively. Results DHA could significantly inhibit the structural remodeling of small pulmonary arterial induced by MCT. Compared with the normal group,the expressions of NFATc1 protein and mRNA were remarkably increased in MCT group. Compared with MCT group,the expressions of NFATc1 protein and mRNA were decreased significantly in DHA-treated group. Conclusions DHA reverses the development of pulmonary hypertention induced by MCT in rats. The mechanism may be related to reduction of the expression of NFATc1.