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目的探讨人工合成E-选择素对大鼠局灶性脑缺血/再灌注(I/R)损伤后脑组织一氧化氮合酶(NOS)及血清一氧化氮(NO)含量的影响。方法采用改良的Zea Longa法建立脑I/R损伤模型。66只雄性SD大鼠随机分为对照组、模型组和人工合成E-选择素治疗组(治疗组)。治疗组大鼠采用股静脉注射人工合成E-选择素10 mg·kg-1。应用硝酸盐还原法测定血清中NO含量和免疫组化法检测缺血区脑组织神经型一氧化氮合酶(nNOS)、诱导型一氧化氮合酶(iNOS)阳性细胞数。结果①NO:以对照组NO含量为正常生理数据,模型组脑缺血2 h/再灌注2~24 h NO含量呈上升趋势,24 h时达高峰,72 h有所降低但仍高于对照组,各时间点与对照组比较明显增高(P<0.01);治疗组NO变化趋势同模型组,NO含量较模型组减少(P<0.05),较对照组增多(P<0.01)。②NOS:以对照组nNOS、iNOS阳性细胞数为正常生理数据,模型组nNOS阳性细胞在脑缺血2 h/再灌注2 h后开始表达,12 h达高峰,至24 h开始降低,各时间点与对照组比较明显增高(P<0.01);模型组iNOS阳性细胞在脑缺血2 h/再灌注2 h开始出现,并持续增多,随时间延长呈上升趋势,24h达高峰,至72 h出现下降,各时间点与对照组比较明显增多(P<0.01);治疗组各时间点nNOS、iNOS阳性细胞变化趋势同模型组,但较模型组减少(P<0.05),较对照组增多(P<0.01)。结论大鼠脑I/R损伤后脑组织NOS活性表达增多,NO浓度升高导致脑组织损伤;人工合成E-选择素通过降低NOS表达,减少NO释放、减轻炎症反应和脑I/R损伤,起脑保护作用。
Objective To investigate the effects of synthetic E-selectin on the levels of nitric oxide synthase (NOS) and serum nitric oxide (NO) in brain tissue after focal cerebral ischemia / reperfusion (I / R) injury in rats. Methods Brain I / R injury model was established by modified Zea Longa method. Sixty-six male Sprague-Dawley rats were randomly divided into control group, model group and synthetic E-selectin group (treatment group). The rats in the treatment group were injected with synthetic E-selectin 10 mg · kg-1 via the femoral vein. NO content in serum was determined by nitrate reduction method and immunohistochemical method was used to detect the expression of neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) positive cells in ischemic brain tissue. Results NO: The NO content in the control group was normal physiological data. The content of NO in the model group increased from 2 h after reperfusion and from 2 to 24 h after reperfusion, reaching the peak at 24 h, decreasing at 72 h but still higher than that of the control group (P <0.01). The change trend of NO in treatment group was lower than that in model group and NO group (P <0.05), which was higher than that in control group (P <0.01). ②NOS: The number of nNOS and iNOS positive cells in the control group was normal physiological data. The expression of nNOS positive cells in the model group started at 2 h after cerebral ischemia / 2 h after reperfusion, peaked at 12 h, and began to decrease at 24 h. At each time point (P <0.01). The iNOS positive cells in model group began to appear at 2 h after ischemia / reperfusion and continued to increase, with increasing time, the iNOS positive cells reached the peak at 24 h and reached the peak at 72 h (P <0.01). The changes trend of nNOS and iNOS positive cells in the treatment group at the same time point were the same as those in the model group (P <0.05), and were higher than those in the control group (P <0.01) <0.01). Conclusion The expression of NOS in brain tissue increases after I / R injury in rats. The increased concentration of NO leads to brain injury. Synthesized E-selectin decreases the expression of NOS, reduces the release of NO, and reduces the inflammatory reaction and brain I / R injury Brain protection.