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牛磺酸通过抑制大鼠脑缺血中12/15脂氧合酶途径实现神经保护作用。

Neuroprotection of taurine through inhibition of 12/15 lipoxygenase pathway in cerebral ischemia of rats.

作者信息

Zhang Zhe, Yu Rongbo, Cao Lei

机构信息

a Department of Geriatrics , Weihai Municipal Hospital , Weihai , China.

b Department of Cardiovascular , Weihai Municipal Hospital , Weihai , China.

出版信息

Neurol Res. 2017 May;39(5):453-458. doi: 10.1080/01616412.2017.1297906. Epub 2017 Mar 3.

DOI:10.1080/01616412.2017.1297906
PMID:28256152
Abstract

BACKGROUND

Cerebral ischemia exhibits a multiplicity of pathophysiological mechanisms. Taurine (Tau), an endogenous substance, possesses a number of cytoprotective properties. The aim of the present study was to examine the neuroprotective effect of Tau, through affecting 12/15 lipoxygenase (12/15-LOX) signal pathway in an acute permanent middle cerebral artery occlusion (MCAO) model of rats.

METHODS

Sprague-Dawley rats were randomly divided into 3 groups (n = 10), namely the sham-operated group, MCAO group and Tau group. Tau was intraperitoneally administrated immediately after cerebral ischemia. At 24 h after MCAO, neurological function score, brain water content and infarct volume were assessed. The expression of 12/15-lipoxygenase (12/15-LOX), p38 mitogen-activated protein kinase (p38 MAPK), and cytosolic phospholipase A2 (cPLA2) was measured by Western blot. Enzyme-linked immunosorbent assay was used to evaluate the inflammatory factors TNF-α, IL-1β and IL-6 in serum.

RESULTS

Compared with MCAO group, taurine significantly improved neurological function and significantly reduced brain water content (p < 0.05) and infarct volume (p < 0.05). Consistent with these indices, the overexpressions of 12/15-LOX, p38 MAPK, cPLA2, tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) were significantly decreased in Tau group (p < 0.05).

CONCLUSION

Taurine protected the brain from damage caused by MCAO; this effect may be through down-regulation of 12/15-LOX, p38 MAPK, and cPLA2.

摘要

背景

脑缺血呈现出多种病理生理机制。牛磺酸(Tau)作为一种内源性物质,具有多种细胞保护特性。本研究旨在通过影响大鼠急性永久性大脑中动脉闭塞(MCAO)模型中的12/15脂氧合酶(12/15-LOX)信号通路,来研究牛磺酸的神经保护作用。

方法

将Sprague-Dawley大鼠随机分为3组(n = 10),即假手术组、MCAO组和牛磺酸组。脑缺血后立即腹腔注射牛磺酸。MCAO术后24小时,评估神经功能评分、脑含水量和梗死体积。通过蛋白质免疫印迹法检测12/15-脂氧合酶(12/15-LOX)、p38丝裂原活化蛋白激酶(p38 MAPK)和胞质磷脂酶A2(cPLA2)的表达。采用酶联免疫吸附测定法评估血清中的炎症因子肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)。

结果

与MCAO组相比,牛磺酸显著改善神经功能,显著降低脑含水量(p < 0.05)和梗死体积(p < 0.05)。与这些指标一致,牛磺酸组中12/15-LOX、p38 MAPK、cPLA2、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)的过表达显著降低(p < 0.05)。

结论

牛磺酸可保护大脑免受MCAO所致损伤;这种作用可能是通过下调12/15-LOX、p38 MAPK和cPLA2实现的。

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