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香豆素提取物通过改变脑梗死和急性脑缺血时的炎症介质对脑组织凋亡的影响。

Effect of Melilotus officinalis extract on the apoptosis of brain tissues by altering cerebral thrombosis and inflammatory mediators in acute cerebral ischemia.

机构信息

Department of Neurology, Shanxian Dongda Hospital, Shanxian 274300, Shandong, China.

Department of Neurology, Chengwu Hospital of Traditional Chinese Medicine, Chengwu 274200, Shandong, China.

出版信息

Biomed Pharmacother. 2017 May;89:1346-1352. doi: 10.1016/j.biopha.2017.02.109. Epub 2017 Mar 18.

Abstract

Present investigation evaluates the protective effect of Melilotus officinalis (MO) extract on the brain tissues in acute cerebral ischemia. Acute cerebral ischemia was induced by occlusion of carotid artery and rats with cerebral ischemia were treated with MO (100, 250 & 500mg/kg) for the duration of three days. Cerebral ischemia was confirmed by estimating infract volume and neurological deficit score. Moreover biochemical parameters in plasma such as 6-keto-PGF1α and TXB2 and concentration of cytokine, oxidative stress, apoptosis ratio and protein expressions of Bcl2 & Bax were estimated in the brain tissues. It was observed that treatment with MO significantly (p<0.01) decreases the infract volume and neurological deficit score than negative control group. There was significant decrease (p<0.01) in the oxidative stress and cytokine in the brain tissues and increase in the plasma concentration of 6-keto-PGF1α in MO treated group of rats compared to negative control group. Plasma concentration of TXB 2 was significantly enhanced in MO treated group compared to negative control group of rats. It was also found that treatment with MO ameliorates the apoptosis induced by cerebral ischemia. Present study concludes that MO ameliorates apoptosis of brain tissues in cerebral ischemic rats by decreasing cerebral thrombosis, oxidative stress and inflammatory mediators.

摘要

本研究评估了草木樨(MO)提取物对急性脑缺血脑组织的保护作用。通过颈总动脉闭塞诱导急性脑缺血,并用 MO(100、250 和 500mg/kg)治疗脑缺血大鼠 3 天。通过评估梗死体积和神经功能缺损评分来确认脑缺血。此外,还评估了血浆中的生化参数,如 6-酮-PGF1α 和 TXB2,以及脑内细胞因子、氧化应激、细胞凋亡率和 Bcl2 和 Bax 蛋白表达的浓度。结果显示,与阴性对照组相比,MO 治疗组的梗死体积和神经功能缺损评分显著降低(p<0.01)。与阴性对照组相比,MO 治疗组大鼠脑组织中的氧化应激和细胞因子显著减少(p<0.01),血浆中 6-酮-PGF1α 的浓度增加。与阴性对照组相比,MO 治疗组大鼠的 TXB2 血浆浓度显著升高。研究还发现,MO 治疗可改善脑缺血引起的细胞凋亡。本研究得出结论,MO 通过减少脑血栓形成、氧化应激和炎症介质来改善脑缺血大鼠的脑组织细胞凋亡。

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