【摘要】 目的:探讨N-乙酰半胱氨酸(NAC)对慢性间歇缺氧(CIH)模型大鼠海马组织氧化应激及海马神经元凋亡的影响。方法:30只雄性Wistar大鼠随机分为慢性缺氧组、NAC治疗组及正常对照组3组,每组10只。采用化学比色法测定海马组织丙二醛(MDA)、超氧化物歧化酶(SOD)水平,同时应用免疫组化方法检测海马CA1区磷酸化JNK(p-JNK)表达水平,应用TUNEL法检测海马CA1区神经元凋亡率。结果:NAC治疗组MDA水平低于CIH组(1.71±0.43vs1.37±0.26,P<0.05)、SOD活性高于CIH组(44.94±14.01vs57.66±14.07,P<0.05),p-JNK表达水平低于CIH组(0.53±0.10vs0.39±0.16,P<0.05),海马神经元凋亡率显著低于CIH组(0.32±0.18vs0.20±0.11,P<0.05)。结论:NAC能抑制慢性间歇缺氧导致的氧化应激,从而影响JNK信号转导通路,减少海马神经元凋亡。更多还原

【Abstract】 AIM:To investigate the effect of N-acetylcystein(NAC)on oxidant stress,neuron apoptosis in the hippocampal CA1 region of rats exposured to chronic intermittent hypoxia(CIH).METHODS:30 healthy male Wistar rats were randomly divided into three groups of 10 each,a CIH group,a NAC therapeutic group and a control group.The levels of MDA and SOD were detected by colorimetric method.Immunohistochemistry was used to examine the expression of p-JNK and TUNEL was used to detect the neuron apoptosis in the hippocampal CA1 region.RESULTS:The level of MDA in NAC group were lower than that in CIH group[(1.71±0.43)μmol/g protein vs(1.37±0.26)μmol/g protein,P<0.05)].The activity of SOD in NAC group was higher than that in CIH group[(44.94±14.01)103 NU/g protein vs(57.66±14.07)103 NU/g protein,P<0.05)].The expression of p-JNK protein and the apoptotic indices [(0.39±0.16),(0.20±0.11)] in NAC group were significantly lower than those in CIH group [(0.53±0.10),(0.32±0.18),all P<0.05].CONCLUSION:NAC protects hippocampal neuron from apoptosis by suppressing the oxidant stress in the hippocampal CA1 region and inhibiting the activation of JNK signaling pathway.更多还原