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姜黄素通过抑制JNK/c-Jun信号通路减轻大鼠蛛网膜下腔出血后的早期脑损伤

[Curcumin alleviates early brain injury following subarachnoid hemorrhage in rats by inhibiting JNK/c-Jun signal pathway].

作者信息

Li Xia, Zhu Ji

机构信息

Department of Neurosurgery, First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

Department of Neurosurgery, First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China. *Corresponding author, E-mail:

出版信息

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2018 Mar;34(3):225-229.

PMID:29773103
Abstract

Objective To investigate the inhibitory effect of curcumin on early brain injury following subarachnoid hemorrhage (SAH) by inhibiting JNK/ c-Jun signal pathway. Methods Sixty adult male SD rats were randomly divided into four groups: sham operation group (sham group), SAH group, SAH group treated with 100 mg/(kg.d) curcumin and SAH group treated with 200 mg/(kg.d) curcumin, with 15 rats in each group. Endovascular puncture was used to induce SAH model. Nissl staining was used to test whether neurons were broken. TUNEL staining was used to detect apoptosis. Immunohistochemistry was used to investigate the expression of caspase-3. Western blot analysis was used to detect the expressions of p-JNK, JNK, p-c-Jun, c-Jun, and caspase-3. Results Nissl staining indicated the decrease of Nissl bodies in SAH group, but increase of Nissl bodies in SAH group treated with curcumin. TUNEL staining showed that there were more apoptotic neurons in SAH group compared with sham group, while apoptotic neurons decreased after the treatment with curcumin, more obviously in the group treated with 200 mg/(kg.d) curcumin. The expressions of p-JNK, JNK, p-c-Jun, c-Jun, and caspase-3 were up-regulated in SAH group compared with sham group. However, the expressions of those proteins were down-regulated after the treatment with curcumin, especially by higher-dose curcumin treatment. Conclusion Curcumin might suppress early brain injury after SAH by inhibiting JNK/c-Jun signal pathway and neuron apoptosis.

摘要

目的 通过抑制JNK/c-Jun信号通路,探讨姜黄素对蛛网膜下腔出血(SAH)后早期脑损伤的抑制作用。方法 将60只成年雄性SD大鼠随机分为四组:假手术组(sham组)、SAH组、100 mg/(kg·d)姜黄素治疗的SAH组和200 mg/(kg·d)姜黄素治疗的SAH组,每组15只。采用血管内穿刺法诱导SAH模型。用尼氏染色检测神经元是否破碎。用TUNEL染色检测细胞凋亡。用免疫组织化学法研究caspase-3的表达。用蛋白质免疫印迹分析检测p-JNK、JNK、p-c-Jun、c-Jun和caspase-3的表达。结果 尼氏染色显示SAH组尼氏体减少,而姜黄素治疗的SAH组尼氏体增加。TUNEL染色显示,与假手术组相比,SAH组凋亡神经元更多,而姜黄素治疗后凋亡神经元减少,在200 mg/(kg·d)姜黄素治疗组更明显。与假手术组相比,SAH组p-JNK、JNK、p-c-Jun、c-Jun和caspase-3的表达上调。然而,姜黄素治疗后这些蛋白的表达下调,尤其是高剂量姜黄素治疗。结论 姜黄素可能通过抑制JNK/c-Jun信号通路和神经元凋亡来抑制SAH后的早期脑损伤。

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