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氢生理盐水抑制脑缺血再灌注损伤后神经元细胞凋亡,抑制 p38 丝裂原活化蛋白激酶-半胱氨酸天冬氨酸蛋白酶 3 信号通路。

Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen‑activated protein kinase‑caspase‑3 signaling pathway following cerebral ischemia‑reperfusion injury.

机构信息

Department of Anesthesiology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China.

出版信息

Mol Med Rep. 2017 Oct;16(4):5321-5325. doi: 10.3892/mmr.2017.7294. Epub 2017 Aug 21.

Abstract

Cerebral ischemia‑reperfusion injury (CIRI) is a serious pathological disease that is associated with a high rate death and disability. Saturated hydrogen (H2) saline exhibits brain protective functions through anti‑inflammatory, antioxidant and antiapoptotic effects. The present study investigated the potential treatment effects of H2 on CIRI. In addition, the potential protective mechanisms of H2 in the prevention of CIRI were investigated. Adult, male Sprague‑Dawley rats (n=60) were randomly divided into the following three groups: Sham‑operated group; IR group; and IR + H2 group (0.6 mmol/l, 0.5 ml/kg/day). Hematoxylin and eosin, and TUNEL staining were performed for histopathological analysis and investigation of apoptosis, respectively. In addition, the protein expression of caspase‑3, p38 mitogen‑activated protein kinase (MAPK) and phosphorylated‑p38 MAPK in the cortex were measured by western blotting analysis. These results demonstrated that H2 significantly reduced the number of apoptotic cells, and the protein expression of p38 MAPK and caspase‑3, compared with the IR group. These effects may be associated with the p38MAPK signaling pathway.

摘要

脑缺血再灌注损伤(CIRI)是一种严重的病理疾病,与高死亡率和高残疾率相关。饱和氢气(H2)盐水通过抗炎、抗氧化和抗凋亡作用表现出脑保护功能。本研究探讨了 H2 治疗 CIRI 的潜在作用。此外,还研究了 H2 预防 CIRI 的潜在保护机制。成年雄性 Sprague-Dawley 大鼠(n=60)随机分为以下三组:假手术组;IR 组;IR+H2 组(0.6mmol/l,0.5ml/kg/天)。进行苏木精和伊红(H&E)及 TUNEL 染色,分别用于组织病理学分析和细胞凋亡检测。此外,通过蛋白质印迹分析测量皮质中 caspase-3、p38 丝裂原活化蛋白激酶(p38MAPK)和磷酸化-p38MAPK 的蛋白表达。这些结果表明,与 IR 组相比,H2 可显著减少细胞凋亡数量,以及 p38MAPK 和 caspase-3 的蛋白表达。这些作用可能与 p38MAPK 信号通路有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd76/5647063/55886771c5d9/MMR-16-04-5321-g00.jpg

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