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目的:从线粒体角度观察参知健脑方对缺氧致认知功能障碍大鼠线粒体损伤的保护机制的研究。方法:将老年大鼠随机分为3组,建立缺氧致线粒体损伤的认知功能障碍模型组以及参知健脑方(SZJ)干预组,并用Morris水迷宫对大鼠的学习记忆能力进行检测。采用酶联免疫吸附法(ELISA)检测线粒体细胞色素氧化酶(COX)的活性、8羟基脱氧鸟苷(8-OHdG)、β-淀粉样前体蛋白(βAPP)及β-淀粉样蛋白(Aβ_(1-42))的含量,观察4个指标与认知功能障碍之间的关联性,进而观察缺氧对模型组脑线粒体的影响及SZJ干预组对脑线粒体的保护作用。结果:持续低压缺氧造模脑组织中APP、Aβ_(1-42)含量模型组与正常组、SZJ干预组间均有统计学意义(P<0.01),8-OHdG含量模型组与正常组、SZJ干预组间比较有统计学意义(P<0.01),SZJ干预组与正常组间比较有统计学意义(P<0.05),COX含量正常组与模型组间比较有统计学意义(P<0.01)、模型组与SZJ干预组比较有统计学意义(P<0.05)。结论:参知健脑方可以抑制APP、Aβ_(1-42)的积累、DNA氧化损伤、增强脑线粒体COX的活性,从而保护线粒体发挥神经保护作用,进一步改善缺氧对认知功能障碍学习记忆能力的影响为参知健脑方的临床应用提供实验支持。
AIM: To observe the protective mechanism of Shenzhijiannao on the mitochondrial damage induced by hypoxia in cognitive impairment rats from the perspective of mitochondria. Methods: The aged rats were randomly divided into three groups: model group of hypoxia-induced mitochondrial dysfunction and cognitive intervention group of Shenzhijiangyan (SZJ) were established. The learning and memory abilities of rats were detected by Morris water maze . The activity of mitochondrial cytochrome oxidase (COX) was measured by enzyme-linked immunosorbent assay (ELISA). The activity of 8-OHdG, β-APP and Aβ_ (1-42)). The correlation between the four indexes and cognitive dysfunction was observed. Then the effect of hypoxia on the mitochondria of model group and the protective effect of SZJ intervention group on mitochondria were observed. Results: The levels of APP and Aβ 1-42 in the model group were significantly lower than those in the normal group and the SZJ intervention group (P 0.01). The levels of 8-OHdG in the model group were significantly lower than those in the normal group (P <0.01). There was significant difference between SZJ intervention group and normal control group (P <0.05). The COX content of normal control group and model group was statistically significant (P < 0.01). There was significant difference between model group and SZJ intervention group (P <0.05). Conclusion: Shenzhijiannao can inhibit the accumulation of APP, Aβ 1-42, DNA oxidative damage and enhance the activity of mitochondrial COX in order to protect mitochondria from neuroprotection and further improve the learning and memory of cognitive dysfunction The influence of the ability to provide experimental support for the clinical application of Shenzhi Jiannao Fang.