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目的观察L-精氨酸(L-Arg)和氨基胍(AG)对大鼠局灶性脑缺血组织中一氧化氮(NO)含量的影响,探讨NO对脑缺血再灌注损伤的作用及机制。方法将60只大鼠随机分为假手术组、模型组、L-Arg组和AG组,每组15只。L-Arg组、AG组、模型组和假手术组用线栓法建立大鼠局灶性脑缺血(MCAO)模型后,L-Arg组按500mg·kg-1腹腔注射1mLL-Arg注射液;AG组按100mg·kg-1术后腹腔注射1mLAG注射液;模型组和假手术组术后腹腔注射1mL灭菌生理盐水。观察缺血再灌注后12、24、72h大鼠行为学改变,血清中NO浓度和脑内一氧化氮合酶(NOS)分布的变化。结果与模型组相比,L-Arg组在缺血再灌注12h行为学评分显著降低(P<0.05),AG组在缺血再灌注24h行为学评分显著降低(P<0.05);AG组在缺血再灌注12h行为学评分高于L-Arg组(P<0.05)。与假手术组相比,模型组、L-Arg组和AG组缺血再灌注12、24、72h的NO含量均显著增加(P<0.05);与模型组相比,L-Arg组缺血再灌注12h的N0含量显著升高(P<0.05),AG组缺血再灌注24h的NO含量显著降低(P<0.05)。缺血再灌注12和24h,AG组的NO含量均显著低于L-Arg组(P<0.05);与假手术组相比,缺血再灌注12、24、72h的模型组、L-Arg组和AG组的iNOS阳性细胞均显著增加(P<0.05);与模型组相比,缺血再灌注12、24、72h的L-Arg组iNOS阳性细胞数差别无统计学意义(P>0.05);但AG组在3个时间点的iNOS阳性细胞数均显著低于模型组(P<0.05);AG组在3个时间点的iNOS阳性细胞数均低于L-Arg组(P<0.05)。结论脑缺血再灌注损伤后脑组织内NO和NOS的表达随时间动态变化,且NO在参与缺血性脑损伤过程中可能具有双重作用。L-Arg、AG通过不同的作用机制对大鼠局灶性脑缺血再灌注损伤具有保护作用。
Objective To observe the effects of L-arginine (Arg) and aminoguanidine (AG) on the content of nitric oxide (NO) in focal cerebral ischemia in rats and the effect of nitric oxide on cerebral ischemia-reperfusion injury And mechanism. Methods Sixty rats were randomly divided into sham operation group, model group, L-Arg group and AG group, 15 rats in each group. The rats in L-Arg group, AG group, model group and sham operation group were subjected to focal cerebral ischemia (MCAO) by thread occlusion. The mice in L-Arg group were injected intraperitoneally with 1 mg L-Arg The rats in AG group were given intraperitoneal injection of 1 mL AG 100 mg · kg -1. The model group and sham operation group were intraperitoneally injected with 1 mL sterilized saline. The changes of behavioral changes, NO concentration in serum and the distribution of nitric oxide synthase (NOS) in brain were observed at 12, 24, 72 h after ischemia / reperfusion. Results Compared with the model group, the behavioral score of L-Arg group was significantly lower at 12h after ischemia-reperfusion (P <0.05), while the score of behavior at AG group was significantly lower at 24h after reperfusion (P <0.05) Behavioral scores at 12h after ischemia-reperfusion were higher than those in L-Arg group (P <0.05). Compared with the sham-operated group, NO content in model group, L-Arg group and AG group at 12, 24 and 72h after ischemia / reperfusion were significantly increased (P <0.05). Compared with model group, L-Arg group The content of NO at 12h after reperfusion was significantly increased (P <0.05), and the content of NO at 24h after reperfusion was significantly decreased (P <0.05). The levels of NO in AG group were significantly lower than those in L-Arg group at 12 and 24 h after ischemia / reperfusion (P <0.05) (P <0.05). Compared with the model group, the number of iNOS positive cells in L-Arg group at 12, 24 and 72 h after ischemia-reperfusion was not significantly different (P> 0.05 ). However, the number of iNOS positive cells in AG group at 3 time points was significantly lower than that in model group (P <0.05). The number of iNOS positive cells in AG group at 3 time points was lower than that in L-Arg group ). Conclusion The expression of NO and NOS in brain tissue after cerebral ischemia-reperfusion injury changes dynamically with time, and NO may play a dual role in the process of ischemic brain injury. L-Arg and AG have protective effects on focal cerebral ischemia-reperfusion injury through different mechanisms of action.