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丹皮酚对大鼠脑缺血再灌注损伤后TLR4及神经细胞凋亡的影响
引用本文:杨青,武继彪,张岫美.丹皮酚对大鼠脑缺血再灌注损伤后TLR4及神经细胞凋亡的影响[J].中国药学杂志,2010,45(17):1327-1330.
作者姓名:杨青  武继彪  张岫美
作者单位:1.山东大学医学院药理学研究所,济南 250012;2.山东中医药高等专科学校,山东 莱阳 260062
摘    要: 目的 观察丹皮酚对大鼠局灶性脑缺血再灌注损伤后 Toll样受体4(TLR4)和神经细胞凋亡的影响,并探讨其作用机制。方法 大鼠随机分为假手术组、脑缺血再灌注模型组、尼莫地平组(0.4 mg·kg-1)、丹皮酚组(15、30 mg·kg-1)。采用线栓法阻塞大脑中动脉建立大鼠局灶性脑缺血再灌注模型。通过 HE染色观察大鼠大脑皮层区细胞损伤程度,免疫组化法检测缺血侧脑组织 TLR4表达的变化,酶联免疫吸附法测定血清白细胞介素6(IL-6)含量,流式细胞仪检测神经细胞凋亡。结果 丹皮酚可明显改善大鼠皮层区细胞损伤,减少 TLR4的表达、降低血清中 IL-6含量,减轻神经细胞凋亡率。结论 丹皮酚能减轻缺血再灌注脑组织损伤程度、降低神经细胞凋亡率,机制可能与抑制脑组织内 TLR4表达有关。

关 键 词:丹皮酚  缺血再灌注  Toll样受体4  白介素6
收稿时间:2012-01-01;

Effect of Paeonol on TLR4 and Apoptosis in Rats with Focal Cerebral Ischemia-Reperfusion Injury
YANG Qing,WU Ji-biao,ZHANG Xiu-mei.Effect of Paeonol on TLR4 and Apoptosis in Rats with Focal Cerebral Ischemia-Reperfusion Injury[J].Chinese Pharmaceutical Journal,2010,45(17):1327-1330.
Authors:YANG Qing  WU Ji-biao    ZHANG Xiu-mei
Institution:1. Department of Pharmacology, School of Medicine, Shandong University, Jinan 250012, China; 2. Shandong Traditional Chinese Medical School, Laiyang 260062, China
Abstract:OBJECTIVE To investigate the effects of paeonol on Toll-like receptor (TLR4) and neuron apoptosis after focal cerebral ischemia-reperfusion injury and its possible mechanism in rats. METHODS 100 Rats were randomly divided into sham group, ischemia-reperfusion group, nimodipine group, and paeonol groups (15 and 30 mg·kg-1). Focal cerebral ischemic model was established by middle cerebral artery occlusion (MCAO). The morphological changes of cerebral cortical neurons through HE staining were observed. The content of IL-6 in serum was measured by ELISA. The apoptosis was detected by flow cytometry. RESULTS Paeonol decreased neuronal edema and neuronal apoptosis of cortex, reduced the content of IL-6 in serum and TLR4 in brain. CONCLUSION Paeonol could relieve brain damage induced by focal cerebral ischemia-reperfusion, and decrease neuronal apoptosis. The effects may be related to the decrease of TLR4 content in brain.
Keywords:Paeonol  ischemia-reperfusion  TLR4  IL-6  apoptosis
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