医学分子生物学杂志 ›› 2022, Vol. 19 ›› Issue (3): 235-239.doi: 10.3870/j.issn.1672-8009.2022.03.010

• 论著 • 上一篇    下一篇

杜仲水提物对脑梗死大鼠神经细胞凋亡的影响

  

  1. 湖北医药学院附属国药东风总医院神经内科 湖北省十堰市, 442008
  • 出版日期:2022-05-31 发布日期:2022-06-20
  • 基金资助:
     2019 年湖北省卫生健康科研基金资助 (No: WJ2019F069)

Effect of Eucommia Water Extract on Apoptosis of Neurons in Rats with Cerebral Infarction

  1. Department of Neurology, Dongfeng General Hospital of Sinopharm, Hubei Medical College, Shiyan, Hubei, 442008, China 
  • Online:2022-05-31 Published:2022-06-20

摘要: 目的 探索杜仲水提物对脑梗死大鼠神经细胞凋亡的影响。 方法 将 40 只大鼠随机分为对照 组、 模型组、 杜仲水提物组和 Ravoxertinib 组, 各 10 只。 HE 染色检测大鼠大脑皮质损伤、 TUNEL 染色检 测大鼠大脑皮质细胞凋亡、 ELISA 法检测氧化应激指标超氧化物歧化酶 ( SOD)、 丙二醛 (MDA) 和半胱 氨酸天冬氨酸蛋白酶 3 (Caspase-3) 水平; Western 印迹检测大鼠大脑皮质中 ERK1 / 2 信号通路。 结果 HE 染色结果显示, 对照组大鼠脑组织无明显病理变化, 模型组大鼠脑组织病理损伤显著增加 (P< 0. 05), 杜 仲水提物组和 Ravoxertinib 组大鼠脑组织病理损伤明显减轻 (P< 0. 05); 与对照组大鼠相比, 模型组大鼠神 经细胞凋亡率、 Caspase-3 和 MDA 水平、 p-ERK1 / 2 / ERK1 / 2 和 Bax 表达水平明显升高, SOD 水平明显降低 (P< 0. 05); 与模型组大鼠比较, 杜仲水提物组大鼠和 Ravoxertinib 组大鼠神经细胞凋亡率、 Caspase-3 和 MDA 水平、 p-ERK1 / 2 / ERK1 / 2 和 Bax 表达水平明显下降, SOD 含量明显上升 (P< 0. 05); 与杜仲水提物 组大鼠比较, Ravoxertinib 组大鼠上述指标无明显差异 (P > 0. 05)。 结论 杜仲水提物通过调控 ERK1 / 2 信 号通路, 改变大鼠脑组织神经细胞生物学行为, 调节氧化应激反应, 从而对脑梗死发挥治疗作用。 

关键词: 脑梗死, 杜仲水提物, 神经细胞凋亡

Abstract: Objective To explore the effect of eucommia water extract on the apoptosis of neurons in rats with cerebral infarction. Methods A total of 40 rats were randomly divided into control group, model group, eucommia water extract group and Ravoxertinib group, with 10 rats in each group. The cerebral cortex damage was determined by HE staining. The apoptosis of cerebral cortex cells was assayed by TUNEL staining. The levels of oxidative stress indexes [ superoxide dismutase (SOD), malondialdehyde (MDA), cysteine aspastic protease 3 (Caspase-3)] were measured by ELISA. The extracellular signal regulated kinase 1 / 2 (ERK1 / 2) signaling in cerebral cortex was detected by Western blotting. Results HE staining showed no obvious pathological changes of brain tissues in control group, but significant pathological damage of brain tissues in model group (P < 0. 05). Eucommia water extract group and Ravoxertinib could significantly relieve the damage of brain tissues (P < 0. 05). The apoptosis rate of neurons, the levels of Caspase-3 and MDA, and the expression levels of p-ERK1 / 2 / ERK1 / 2 and Bax were significantly increased and the level of SOD was significantly decreased in model group compared with the control group (P< 0. 05). These indexes were significantly reversed in eucommia water extract group and Ravoxertinib group as compared with the model group (P< 0. 05). There was no significant difference in the indexes between the eucommia water extract group and Ravoxertinib group (P > 0. 05). Conclusion Eucommia water extract can regulate biological behaviors of neurons and oxidative stress response in brain tissues by regulating ERK1 / 2 signaling pathways, thereby playing roles in the treatment of cerebral infarction in rats. 

Key words: cerebral infarction, eucommia water extract, neuron apoptosis

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