| N-乙酰L-半胱氨酸预处理对大鼠局灶性脑缺血再灌注损伤的保护机制 |
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| 引用本文： | 胡安康,;顾建红,;刘宗平.N-乙酰L-半胱氨酸预处理对大鼠局灶性脑缺血再灌注损伤的保护机制[J].兽医大学学报,2014(8):1332-1336. |
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| 作者姓名： | 胡安康 ;顾建红 ;刘宗平 |
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| 作者单位： | [1]徐州医学院试验动物中心,江苏徐州221002; [2]扬州大学兽医学院,江苏扬州225009 |
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| 基金项目： | 江苏省自然科学基金资助项目（SBK201121584）; 江苏省高校自然科学基金资助项目（13KJD180003）; 江苏省高校优势学科建设工程资助项目 |
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| 摘 要： | 制备大鼠局灶性脑缺血再灌注实验模型,通过N-乙酰L-半胱氨酸（NAC）预处理对脑缺血再灌注损伤的保护作用,探索脑梗死病理过程及药物治疗途径。NAC预处理21d,利用栓线法建立大鼠大脑中动脉栓塞模型,造模后24h进行神经症状评分,TTC染色,检测血浆MDA、GSH含量,观察大脑皮质细胞凋亡情况及凋亡相关蛋白Bcl-2、Bax的表达。结果显示,通过神经症状评分和TTC染色判定大鼠局灶性脑缺血实验模型建立成功。与对照组相比,NAC预处理组（100mg·kg^-1）大鼠血浆中MDA含量显著降低（P〈0.05）,GSH含量显著升高（P〈0.05）;NAC模型组细胞凋亡率及Bax/Bcl-2比值明显低于对照组。结果表明,NAC通过改善氧化应激状态,调控凋亡蛋白Bcl-2、Bax表达,从而对大鼠脑缺血再灌注损伤具有一定的保护作用。
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| 关 键 词： | 局灶性脑缺血 N-乙酰L-半胱氨酸(NAC) TTC染色 细胞凋亡 |
N-acetyl L-cysteine preconditioning protection from focal cerebral ischemia reperfusion injury in rat |
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| Institution: | HU An-kang , GU Jian hong , LIU Zong-ping ( 1. College, Xuzhou, J iangsu 221002, China ; 2. College Laboratory Animal Center, Xuzhou of Veterinary Medicine ,Yangzhou Medical University ,Yangzhou , J iangsu 225009, China ) |
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| Abstract: | Through the research of N-acetyl L cysteine preconditioning on cerebral ischemia, exploring cerebral infarction pathological process and treatment approaches. The treated mouse received continuous intraperitoneal injection with different doses of NAC（50,100,150μmol·kg^-1） for 21 clays,and then was subjected to focal cerebral ischemia damage induced by a middle cerebral artery occlusion（MCAO） for 24 h. The neurological deficit,pathological change and infarct scope were deterinimed by Bederson＇5 score, and TTC staining. The activity of MDA and GSH in the blood were detected by colorimetric method flow cytometry was used for determination of the cortical neuronal apoptosis;the expression of Bcl-2 and gax in the cortical neuron were detected by Western blot. Focal cerebral ischemia models was established. Levels of MDA in the NAC groups were lower than those in the vechicl group（P〈0.05）. Meanwhile,content of GSH in the NAC groups were siginificantly increased （P〈0.05） ;NAC significantly decreased the apoptosis of neu ral cells,increased the expression of Bcl-2 and reduced the expression of Bax and increased Bcl-2/ Bax expression ratio. NAC has protective effects on focal cerebral ischemia damage and its mechanism may be related to resist oxidative damage,reduce acidosis and increase the content of GSH in the blood,depress cell apoptosis through affecting the expression of the apoptosis-related protein, such as Bcl-2 and Bax. |
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| Keywords: | focal cerebral ischemia N-acetyl L-cysteine TTC staining apoptosis |
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