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[亚硒酸钠对大鼠海马神经元脑缺血再灌注损伤的保护作用]

[Protective effect of Na2SeO3 against cerebral ischemia-reperfusion injury to the hippocampal neurons in rats].

作者信息

Wang Guang-sheng, Geng De-qin, Wang Yuang-wei, Chen Xiao-dong, Yang Tong-hui, Chang Chun-hong

机构信息

Department of Neurology, Shuyang peoples Hospital of Jiangsu province, Shuyang 223600, China.

出版信息

Nan Fang Yi Ke Da Xue Xue Bao. 2010 Oct;30(10):2336-9.

Abstract

OBJECTIVE

To investigate the protective effects of selenium on rat hippocampal neurons against ischemia-reperfusion (IR) injury.

METHODS

Thirty-two rats were randomly divided into sham-operated group, IR group and selenium-treated group, and in the latter two groups, cerebral IR injury was induced by middle cerebral artery occlusion; Na2SeO3 treatment was administer in selenium-treated group. At 14 days after reperfusion, the brain tissues were harvested from the rats and hippocampal neuron injuries were observed by TUNEL and Methylene Blue staining. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and nerve growth factor (NGF) in the hippocampal tissues were measured by ELISA.

RESULTS

Compared with IR group, the rats in selenium-treated group showed no significant increase in the expression of m-NGF (P>0.05), but pro-NGF expression was significantly increased (P<0.05) in the hippocampal tissue. Na2SeO3 treatment significantly inhibited the expressions of TNF-α and IL-1β and decreased the apoptosis of hippocampal neurons following cerebral IR injury (P<0.05).

CONCLUSION

Selenium produces antiapoptotic effect to protect the hippocampal neurons following cerebral IR injury possibly not by increasing the level of m-NGF but by decreasing the expressions of the inflammatory factors.

摘要

目的

探讨硒对大鼠海马神经元缺血再灌注(IR)损伤的保护作用。

方法

将32只大鼠随机分为假手术组、IR组和硒处理组,后两组采用大脑中动脉闭塞法诱导脑IR损伤;硒处理组给予亚硒酸钠治疗。再灌注14天后,取大鼠脑组织,通过TUNEL和亚甲蓝染色观察海马神经元损伤情况。采用酶联免疫吸附测定法(ELISA)检测海马组织中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和神经生长因子(NGF)的水平。

结果

与IR组相比,硒处理组大鼠海马组织中成熟型NGF(m-NGF)表达无显著增加(P>0.05),但前体NGF(pro-NGF)表达显著增加(P<0.05)。亚硒酸钠治疗显著抑制了TNF-α和IL-1β的表达,并减少了脑IR损伤后海马神经元的凋亡(P<0.05)。

结论

硒可能不是通过提高m-NGF水平,而是通过降低炎症因子的表达来产生抗凋亡作用,从而保护脑IR损伤后的海马神经元。

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