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出 处:《浙江临床医学》2016年第7期1189-1190,共2页Zhejiang Clinical Medical Journal
基 金:国家自然科学基金项目(81270236)
摘 要: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.
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