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目的研究伊达拉奉(3-甲基-1苯基-2-吡唑啉-5-酮)对新生Harlequin(Hq)小鼠缺氧缺血性脑损伤(HIBD)的神经保护作用及可能机制。方法新生9日龄雄性Hq小鼠随机分为伊达拉奉治疗组(n=16)与对照组(n=17)。小鼠在动脉结扎缺氧后分别即刻经腹腔注射伊达拉奉(10 mg/kg)或相同体积9 g/L盐水。采用免疫组织化学法在缺氧缺血(HI)后3 h和24 h检测硝基酪氨酸和脂质过氧化物的形成,分别采用蛋白印迹及荧光分光光度法在HI后24 h测定硝基酪氨酸的形成和半胱天冬酶的活性,HI后72 h采用神经病理学评分和测定梗死体积评价脑损伤的程度。结果HI后大脑皮层、海马、纹状体和丘脑均可见梗死灶,伊达拉奉治疗可明显减少大脑各区域的损伤程度,脑梗死体积与对照组相比减少52.8%(P<0.001)。伊达拉奉治疗可明显减少硝基酪氨酸与脂质过氧化物的形成,但对半胱天冬酶活性无明显影响。结论伊达拉奉对新生鼠HIBD具有神经保护作用,这种保护作用可能与减少自由基的形成有关。
Objective To investigate the neuroprotective effects of idarone (3-methyl-1-phenyl-2-pyrazolin-5-one) on neonatal Harlequin (Hq) mice with hypoxic-ischemic brain damage mechanism. Methods Newborn 9-day-old male Hq mice were randomly divided into two groups: treatment group (n = 16) and control group (n = 17). Mice were injected with idaroflix (10 mg / kg) or the same volume of 9 g / L saline immediately after arterial ligation of hypoxia. The formation of nitrotyrosine and lipid peroxidation was detected by immunohistochemistry at 3 h and 24 h after hypoxia-ischemia (HI), respectively. The expression of nitrotyrosine and lipid peroxidation was measured by Western blotting and fluorescence spectrophotometry at 24 h after HI Tyrosine formation and caspase activity. The severity of brain injury was evaluated by neuropathological score and infarction volume at 72 h after HI. Results After HI, infarction was found in the cerebral cortex, hippocampus, striatum and thalamus. Idallat treatment could significantly reduce the degree of brain damage. The volume of cerebral infarction was decreased by 52.8% (P <0.001) compared with the control group. Idallat treatment significantly reduced nitrotyrosine and lipid peroxidation, but had no significant effect on caspase activity. Conclusions Idaravone has neuroprotective effects on HIBD in neonatal rats. This protective effect may be related to reducing the formation of free radicals.