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p66Shc基因敲除对小鼠缺血缺氧性脑损伤的保护作用
Neuroprotective Effects of p66Shc Knock-out on Hypoxic-ischemic Brain Injury in Mice
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摘要:目的 探讨p66Shc基因敲除对小鼠缺血缺氧性脑损伤(hypoxic-ischemic brain injury, HIBI)的保护作用及可能的机理。方法 将C57小鼠分为假手术组(野生型, sham operation, SO)、HIBI野生型组(hypoxic-ischemic wild type, HIWT)和HIBI-p66Shc基因敲除组(hypoxic-ischemic knock-out, HIKO), 每组20只。采用右侧颈总动脉结扎-浸入低氧环境的方法制备小鼠HIBI模型。随后对各组小鼠神经功能障碍情况、HIBI损伤灶体积、血清神经元特异性烯醇化酶(neuronspecific enolase, NSE)水平和脑组织匀浆中白细胞介素-1β(interleukin-1β, IL-1β)的水平进行测量和比对。结果 HIBI造模24 h后, HIKO组小鼠的神经功能缺损程度评分(1.87±0.30)低于HIWT组小鼠(2.49±0.26), HIKO组小鼠脑梗死灶体积(22.66±4.20)mm3小于HIWT组小鼠(27.31±3.23)mm3, HIKO组小鼠血清NSE含量(8.97±0.74)ng/ml显著低于HIWT组小鼠(11.26±0.68)ng/ml, HIKO组小鼠脑组织IL-1β含量(1.72±0.30)ng/ml显著低于HIWT组小鼠(2.07±0.28)ng/ml, P均 < 0.05。结论 p66Shc基因敲除可通过降低小鼠HIBI发生后脑组织IL-1β的表达, 起到脑保护作用。Abstract:Objective To explore neuroprotective effects of p66Shc knock-out on hypoxic-ischemic brain injury in mice and possible underlining mechanisms.Methods C57 mice were divided into 3 groups:sham-operation group (SO, wild type), hypoxic-ischemic wild type group (HIWT) and hypoxic-ischemic p66Shc knock-out group (HIKO), 20 mice each group. HIBI model making:ligation of the right common carotid artery and then exposure to a hypoxic environment. The neurological dysfunction score, HIBI lesion volume, serum neuron specific enolase (NSE) level and interleukin (IL)-1β level in brain tissue were measured and compared.Results Twenty-four hours after HIBI, the neurological function of HIKO mice was better than that of HIWT mice, the HIBI lesion volume of HIKO mice was smaller than that of HIWT mice, the serum NSE level of HIKO mice was much lower than that of HIWT mice, IL-1β level in the brain tissue of HIKO mice was much lower than that of HIWT mice (all P < 0.05).Conclusion p66Shc knock-out plays an important role in neuroprotective effects on HIBI of mice, possibly through attenuating IL-1β expression in the brain tissue after HIBI.
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