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低剂量辐射诱导 1 型糖尿病小鼠肾 SOD1 的表达和活性。

Low-dose radiation induces renal SOD1 expression and activity in type 1 diabetic mice.

机构信息

Ruian Center of the Chinese-American Research Institute for Diabetic Complications, the Third Affiliated Hospital of the Wenzhou Medical College , Wenzhou.

出版信息

Int J Radiat Biol. 2014 Mar;90(3):224-30. doi: 10.3109/09553002.2014.877174.

DOI:10.3109/09553002.2014.877174
PMID:24397406
Abstract

PURPOSE

Oxidative stress plays a critical role in the pathogenesis of diabetic nephropathy (DN). As an antioxidant, superoxide dismutase (SOD)-1 deficiency exacerbates but SOD1 supplementation prevents diabetes-induced renal damage. Previously, we have demonstrated that repetitive exposure to low-dose radiation (LDR) at 25 mGy significantly prevents DN. Whether this prevention is related to SOD1 expression and activity remains unknown. The aim of the present study was to explore the effects of different methods of LDR treatment on SOD1 expression and activity in the kidneys of diabetic mice.

MATERIALS AND METHODS

C57BL/6J mice were induced with type 1 diabetes using streptozotocin (STZ). Diabetic mice were irradiated with whole-body X-rays at either a single dose of 25 mGy or 75 mGy, or three doses of 25 mGy and then sacrificed at different times. Body weight, blood glucose level, and renal SOD1 expression and activity were measured.

RESULTS

LDR had no impact on the body weights or blood glucose levels of the mice in either the normal or diabetic groups. A single exposure of LDR at 25 mGy did not preserve renal SOD1 expression and activity in diabetic mice, but a single exposure of LDR at 75 mGy or three exposures of LDR at 25 mGy could preserve them.

CONCLUSION

The stimulation of renal SOD1 expression and activity by a single or cumulative LDR of 75 mGy may be one of the preventive mechanisms of DN observed in the previous study.

摘要

目的

氧化应激在糖尿病肾病(DN)的发病机制中起关键作用。超氧化物歧化酶 1(SOD1)作为一种抗氧化剂,其缺乏会加重糖尿病引起的肾损伤,而 SOD1 的补充则可预防。先前我们已经证明,重复暴露于 25mGy 的低剂量辐射(LDR)可显著预防 DN。但这种预防作用是否与 SOD1 的表达和活性有关尚不清楚。本研究旨在探讨不同 LDR 处理方法对糖尿病小鼠肾脏中 SOD1 表达和活性的影响。

材料与方法

采用链脲佐菌素(STZ)诱导 C57BL/6J 小鼠发生 1 型糖尿病。对糖尿病小鼠进行全身 X 射线照射,单次照射剂量为 25mGy 或 75mGy,或三次照射 25mGy,然后在不同时间点处死。测量体重、血糖水平以及肾脏 SOD1 的表达和活性。

结果

LDR 对正常或糖尿病小鼠的体重或血糖水平均无影响。单次 25mGy 的 LDR 照射不能维持糖尿病小鼠肾脏 SOD1 的表达和活性,但单次 75mGy 的 LDR 照射或三次 25mGy 的 LDR 照射可维持其表达和活性。

结论

单次或累积 75mGy 的 LDR 刺激肾脏 SOD1 的表达和活性可能是先前研究中观察到的 DN 预防机制之一。

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