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目的研究亚慢性铝暴露对大鼠海马线粒体的损伤作用及其机制。方法无特定病原体级健康雄性成年SD大鼠60只,按体质量随机分为空白组、对照组和低、中、高剂量组,每组12只。空白组不作任何处理,低、中、高剂量组分别予剂量为0.41、0.81、1.62 mg/kg体质量的麦芽酚铝溶液,对照组予等体积0.9%氯化钠溶液,隔日腹腔注射染毒。连续染毒90 d后,以化学比色法检测大鼠海马组织中钠-钾-三磷酸腺苷酶(Na+-K+-ATP酶)和钙-镁ATP酶(Ca2+-Mg2+-ATP酶)活力,以免疫印迹法检测大鼠海马组织中细胞色素氧化酶4(CoxⅣ)、动力相关蛋白1(Drp1)、视神经萎缩蛋白1(Opa1)、线粒体融合蛋白(Mfn)1和Mfn2表达水平。结果高剂量组大鼠海马组织Na+-K+-ATP酶活力分别低于空白组、对照组和低剂量组(P<0.05);中剂量组大鼠海马组织Ca2+-Mg2+-ATP酶活力低于空白组(P<0.05),高剂量组大鼠海马组织Ca2+-Mg2+-ATP酶活力分别低于其他4组(P<0.05)。中、高剂量组大鼠海马组织中CoxⅣ蛋白相对表达水平分别低于空白组、对照组和低剂量组(P<0.05),Drp1和Mfn2相对表达水平分别高于空白组、对照组(P<0.05),Opa1相对表达水平分别高于空白组、对照组和低剂量组(P<0.05),Mnf1相对表达水平均高于空白组(P<0.05)。结论麦芽酚铝亚慢性染毒可导致大鼠海马组织线粒体损伤,其造成的损伤可能与线粒体动力学的改变有关。
Objective To investigate the effect of subchronic aluminum exposure on rat hippocampal mitochondria and its mechanism. Methods Sixty adult male Sprague-Dawley (SD) rats without specific pathogen were randomly divided into blank group, control group, and low, medium and high dose groups according to body weight, with 12 rats in each group. The blank group was given no treatment, the low, medium and high dose groups were given the doses of 0.41,0.81,1.62 mg / kg body weight of maltol aluminum solution, the control group to an equal volume of 0.9% sodium chloride solution, the next day by intraperitoneal injection . After 90 days of continuous exposure, the activities of Na + -K + -ATPase and Ca2 + -Mg2 + -ATPase in the hippocampus were detected by chemical colorimetry Western blotting was used to detect the expression of CoxⅣ, Drp1, Opa1, Mfn1 and Mfn2 in the hippocampus of rats. Results The Na + -K + -ATPase activity of hippocampus in high-dose group was lower than that in blank group, control group and low-dose group (P <0.05), while the activity of Ca2 + -Mg2 + -ATPase in hippocampus of middle dose group was lower than blank (P <0.05). The activities of Ca2 + -Mg2 + -ATP in the hippocampus of high-dose group were lower than the other four groups (P <0.05). The relative expression levels of Cox ¢ ô in the hippocampus were lower than those in the blank group, the control group and the low dose group (P <0.05), and the relative expression levels of Drp1 and Mfn2 were higher in the middle and high dose groups than those in the blank group and the control group (P < 0.05). The relative expression level of Opa1 was higher than that of blank group, control group and low dose group (P <0.05), and the relative expression level of Mnf1 was higher than that of blank group (P <0.05). Conclusion Subchronic exposure to maltophenolate may result in the damage of mitochondria in hippocampus of rats, which may be related to the change of mitochondrial dynamics.