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[氧化应激在实验性糖尿病神经病变中的作用]

[The role of oxidative stress in experimental diabetic neuropathy].

作者信息

Wang Ling, Zheng Kai-Jun, Dong De-Yong, Sun Yue, Wang Yong-Ming

机构信息

Department of Physiology, Tianjin Medical University, Tianjin 300070, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2008 Feb;24(1):108-11.

Abstract

AIM

To study the role of oxidative stress in the initiation and development of diabetic neuropathy.

METHODS

The diabetic rats were induced with streptozotocin (STZ). The malondialdehyde (MDA) level, total superoxide dismutase (SOD) and Na(+) -K(+) -ATPase activity were measured in the sciatic nerves at various stages of diabetes. The correlation of the MDA level and Na(+) -K(+) -ATPase activity was analyzed in diabetic rats. The pathological changes of sciatic nerve at diabetic various stages were examined by light microscopy.

RESULTS

The MDA level increased significantly in diabetic sciatic nerves as compared to controls at all time intervals. Total SOD activity increased significantly in diabetic sciatic nerves as compared to controls at one month of diabetes and progressively decreased at three/six months of diabetes. Na(+) -K(+) -ATPase activity progressively decreased at three/six months of diabetes. The correlation analysis indicated that the Na(+) -K(+) -ATPase activity was negative correlation with the MDA level in the diabetic rats. Histopathological study of the diabetic sciatic nerves showed that the pathological changes were observed at 3 months of diabetes, the changes were more serious as the diabetic duration was longer.

CONCLUSION

Oxidative stress is found to occur during the early stages of STZ-induced diabetes (no neuropathy) and this state is maintained after initiation of neuropathy. The decreased Na(+) -K(+) -ATPase activity is associated with oxidative stress in the diabetic rats. Therefore, oxidative stress plays an important role in the initiation and development of diabetic neuropathy.

摘要

目的

研究氧化应激在糖尿病神经病变发生及发展过程中的作用。

方法

用链脲佐菌素(STZ)诱导糖尿病大鼠。测定糖尿病不同阶段坐骨神经中的丙二醛(MDA)水平、总超氧化物歧化酶(SOD)和钠钾ATP酶活性。分析糖尿病大鼠中MDA水平与钠钾ATP酶活性的相关性。通过光学显微镜检查糖尿病不同阶段坐骨神经的病理变化。

结果

与对照组相比,糖尿病大鼠坐骨神经中MDA水平在所有时间间隔均显著升高。与对照组相比,糖尿病大鼠坐骨神经中总SOD活性在糖尿病1个月时显著升高,在糖尿病3/6个月时逐渐降低。糖尿病3/6个月时钠钾ATP酶活性逐渐降低。相关性分析表明,糖尿病大鼠中钠钾ATP酶活性与MDA水平呈负相关。糖尿病大鼠坐骨神经的组织病理学研究表明,糖尿病3个月时观察到病理变化,随着糖尿病病程延长变化更严重。

结论

发现氧化应激在STZ诱导的糖尿病早期(无神经病变)即已发生,且在神经病变开始后这种状态持续存在。糖尿病大鼠中钠钾ATP酶活性降低与氧化应激有关。因此,氧化应激在糖尿病神经病变的发生及发展中起重要作用。

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