左旋精氨酸对肺高压大鼠体内炎性因子的影响

目的探讨左旋精氨酸（L—Arg）对肺高压（PH）大鼠体内炎性因子的影响，以进一步了解L—Arg防治PH的分子生物学机制。方法SD雄性大鼠18只随机分为三组（n=6）：对照组（C组）、MCT组（M组）、L-Arg／MCT组（L组）。C组大鼠不做处理，M组和L组大鼠腹腔注射野百合碱诱导PH模型并继续饲养3周；饲养期间L组大鼠每日注射L-Arg，C组和M组每日注射与L—Arg等量的生理盐水。3周时，测大鼠肺动脉压力后取血检测血浆白介素-6（IL-6）、肿瘤坏死因子α（TNF—α）、内皮素-1（ET-1）的含量，然后分析各组炎性因子的变化情况。结果M组大鼠血浆中三种炎性因子含量均较C组升高；L组大鼠血浆中三种炎性因子较M组明显下降。结论L—Arg可以减少PH大鼠体内的炎性因子的含量，进一步阐明L-Arg改善PH的分子生物学机制。

Objective To investigate the effect of L-arginine （ L-Arg ） on inflammatory factors in rats with pulmonary hypertension （ PH ） , and further detect the molecular mechanism of L-Arg on the treatment of PH. Methods 18 SD male rats were randomly divided into three groups （ n=6 ） ： control group （ C ） , MCT group （ M ） , L-Arg/MCT group （ L ） . M group and L group rats were induced PH model by intraperitoneal injection of monocrotaline and fed for 3 weeks. During this periods, daily injections of L-Arg was carried out in L group, group C and M were given a daily injections of saline equal with L-Arg. After 3 weeks, the pulmonary artery pressure of rats was detected before taking blood samples for interleukin -6 （IL-6） , tumor necrosis factor alpha （TNF alpha ） and endothelial endothelin-1 （ET-1） detection. Then the change of inflammatory factors of all groups were analyzed. Results Compared with C, the levels of inflammatory factors were higher in the M group. All inflammatory factors in L group were significantly lower than those in the M group. Conclusion L-Arg can reduce the content of inflammatory factors in PH rats, which further elucidate the molecular biology mechanism of L-Arg on improvement of PH.