| 活性氧簇介导的氧化应激及细胞焦亡在大鼠脑缺血再灌注损伤中的作用 |
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| 引用本文： | 朱文丽,沈晓燕,薛兴亚,吴文婷. 活性氧簇介导的氧化应激及细胞焦亡在大鼠脑缺血再灌注损伤中的作用[J]. 医学分子生物学杂志, 2022, 19(6): 490-495. DOI: 10.3870/j.issn.1672-8009.2022.06.009 |
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| 作者姓名： | 朱文丽 沈晓燕 薛兴亚 吴文婷 |
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| 作者单位： | 陕西省第四人民医院神经内科 西安市, 710043 |
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| 摘 要： | 目的 研究活性氧簇 (ROS) 介导的氧化应激及细胞焦亡在大鼠脑缺血再灌注 ( I/ R) 损伤中的作用。 方法 成年雄性 SD 大鼠分为假手术 ( Sham) 组、 I/ R 组、 ROS 清除剂 N 乙酰半胱氨酸-低剂量(NAC-L) 组、 NAC 中等剂量 (NAC-M) 组、 NAC 高剂量 (NAC-H) 组, 建立脑 I/ R 损伤模型并给予 50、100、 200 mg / kg NAC 腹腔注射干预。 再灌注后 24 h, 评价神经功能, 检测脑梗死面积百分比、 ROS、 丙二醛 (MDA)、 4-羟基壬烯醛 (4-HNE)、 总抗氧化力 (T-AOC)、 裂解型 caspase-1 (Cleaved caspase-1)、 gasdermin D 的 N 端片段 (GSDMD-N)。 结果 I/ R 组脑梗死面积百分比、 ROS、 MDA、 4-HNE 含量、 Cleavedcaspase-1、 GSDMD-N 表达水平均明显增加, T-AOC 含量明显降低 ( P < 0. 05 ); NAC-L 组、 NAC-M 组、NAC-H 组脑梗死面积百分比、 ROS、 MDA、 4-HNE 含量、 Cleaved caspase-1、 GSDMD-N 表达水平均明显降低, T-AOC 含量明显增加 (P< 0. 05) 且 NAC 剂量越高, 上述变化越显著。 结论 ROS 介导的氧化应激及细胞焦亡参与大鼠脑 I/ R 损伤。
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| 关 键 词： | 脑缺血再灌注损伤 活性氧簇 N 乙酰半胱氨酸 氧化应激 细胞焦亡 |
Role of Reactive Oxygen Species Mediated Oxidative Stress and Pyroptosisin Cerebral Ischemia-reperfusion Injury in Rats |
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| ZHU Wenli,SHEN Xiaoyan,XUE Xingya,WU Wenting. Role of Reactive Oxygen Species Mediated Oxidative Stress and Pyroptosisin Cerebral Ischemia-reperfusion Injury in Rats[J]. Journal of Medical Molecular Biology, 2022, 19(6): 490-495. DOI: 10.3870/j.issn.1672-8009.2022.06.009 |
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| Authors: | ZHU Wenli SHEN Xiaoyan XUE Xingya WU Wenting |
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| Affiliation: | Department of Internal Medicine-Neurology, the Fourth People’ s Hospital of Shaanxi, Xi ’ an,710043, China |
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| Abstract: | Objective To study the role of reactive oxygen species (ROS) -mediated oxidative stress and pyroptosis in the cerebral ischemia-reperfusion (I/ R) injury in rats. Methods Adult male SD rats were divided into 5 groups as follows: the sham group, the I/ R group, the ROSscavenger N-acetylcysteine low dose (NAC-L) group, the NAC medium dose (NAC-M) groupand the NAC high dose (NAC-H) group. The cerebral I/ R injury model was established and 50,100 and 200 mg / kg NAC were injected intraperitoneally before ischemia and reperfusion as an intervention. The neurological function was evaluated 24 h after reperfusion, the percentage of cerebralinfarction area, and the levels of ROS, malondialdehyde (MDA), 4-hydroxynonenal (4-HNE)and total antioxidant capacity (T-AOC) were measured. The expression levels of cleaved caspase-1and N-terminal of gasdermin D (GSDMD-N) were detected. Results In the I/ R group, the percentage of cerebral infarction area, the amount of ROS, MDA, 4-HNE, and the expression levelsof cleaved caspase-1 and GSDMD-N were significantly increased, while the amount of T-AOC wassignificantly decreased (P< 0. 05). In the NAC-L, NAC-M and NAC-H groups, the percentage ofcerebral infarction area, the amount of ROS, MDA, 4-HNE, and the expression levels of cleavedcaspase-1 and GSDMD-N were significantly decreased, while the amount of T-AOC was significantlyincreased (P< 0. 05). The changes of the above indexes became more obvious with the increase ofthe NAC dose. Conclusion ROS mediated oxidative stress and pyroptosis are involved in the cerebral I/ R injury in rats. |
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| Keywords: | cerebral ischemia-reperfusion injury,reactive oxygen species,N-acetylcysteine oxidative stress,pyroptosis , |
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