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姜黄素抑制大鼠脑缺血再灌注损伤诱导的内质网应激。

Curcumin inhibits endoplasmic reticulum stress induced by cerebral ischemia-reperfusion injury in rats.

作者信息

Zhu Haiying, Fan Yanxia, Sun Hongyu, Chen Liyan, Man Xiao

机构信息

Department of Neurology, The No. 4 Hospital of Jinan, Jinan, Shandong 250031, P.R. China.

Department of Nursing, The No. 4 Hospital of Jinan, Jinan, Shandong 250031, P.R. China.

出版信息

Exp Ther Med. 2017 Nov;14(5):4047-4052. doi: 10.3892/etm.2017.5040. Epub 2017 Aug 25.

Abstract

The aim of the present study was to observe the dynamic changes of the growth arrest and DNA damage-inducible 153 (GADD153) gene and caspase-12 in the brain tissue of rats with cerebral ischemia-reperfusion injury (CIRI) and the impact of curcumin pretreatment. A total of 60 rats were randomly divided into the normal group (N), the sham operation group (S), the dimethyl sulfoxide control group (D) and the curcumin treatment group (C). For group D and C, 12 (T1), 24 (T2) and 72 h (T3) of reperfusion were performed after 2 h ischemia. The expression levels of GADD153 and caspase-12 in the brain tissue were detected and compared among the groups by immunohistochemistry, immunofluorescence double staining and western blotting. The expression levels of GADD153 and caspase-12 were increased at T1compared with groups N and S, and the expression of caspase-12 peaked at T2 in group D, while GADD153 was increased until T3 in group D. Compared with group D, the expression levels of GADD153 and caspase-12 in group C at T2 and T3 were significantly decreased (P<0.05). Endoplasmic reticulum stress is involved in the pathological process of CIRI. Curcumin may decrease the expression levels of the above two factors, thus exhibiting protective effects against CIRI in rats.

摘要

本研究旨在观察脑缺血再灌注损伤(CIRI)大鼠脑组织中生长停滞和DNA损伤诱导蛋白153(GADD153)基因及半胱天冬酶-12的动态变化以及姜黄素预处理的影响。将60只大鼠随机分为正常组(N)、假手术组(S)、二甲基亚砜对照组(D)和姜黄素治疗组(C)。对于D组和C组,缺血2 h后分别进行再灌注12 h(T1)、24 h(T2)和72 h(T3)。采用免疫组织化学、免疫荧光双染色及蛋白质印迹法检测并比较各组脑组织中GADD153和半胱天冬酶-12的表达水平。与N组和S组相比,T1时GADD153和半胱天冬酶-12的表达水平升高,D组中半胱天冬酶-12的表达在T2时达到峰值,而D组中GADD153在T3时仍持续升高。与D组相比,C组在T2和T3时GADD153和半胱天冬酶-12的表达水平显著降低(P<0.05)。内质网应激参与了CIRI的病理过程。姜黄素可能降低上述两种因子的表达水平,从而对大鼠CIRI发挥保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1e/5647704/052df9c44c6c/etm-14-05-4047-g00.jpg

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