Refined Qingkailing Protects MCAO Mice from Endoplasmic Reticulum Stress-Induced Apoptosis with a Broad Time Window

被引:31
作者
Cheng, Fafeng [1 ]
Zhong, Xianggen [1 ]
Lu, Yi [1 ]
Wang, Xueqian [1 ]
Song, Wenting [2 ]
Guo, Shaoying [1 ]
Wang, Xiaotong [1 ]
Liu, Dantong [1 ]
Wang, Qingguo [1 ]
机构
[1] Beijing Univ Chinese Med, Coll Basic Med, Beijing 100029, Peoples R China
[2] China Acad Chinese Med Sci, Xiyuan Hosp, Beijing 100091, Peoples R China
关键词
CEREBRAL-ARTERY OCCLUSION; RAT MODEL; THERAPEUTIC WINDOW; NITRIC-OXIDE; CELL-DEATH; ISCHEMIA; BAICALIN; DYSFUNCTION; REPERFUSION; INJECTION;
D O I
10.1155/2012/567872
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
In the current study, we are investigating effect of refined QKL on ischemia-reperfusion-induced brain injury in mice. Methods. Mice were employed to induce ischemia-reperfusion injury of brain by middle cerebral artery occlusion (MCAO). RQKL solution was administered with different doses (0, 1.5, 3, and 6mL/kg body weight) at the same time of onset of ischemia, and with the dose of 1.5mL/kg at different time points (0, 1.5, 3, 6, and 9 h after MCAO). Neurological function and brain infarction were examined and cell apoptosis and ROS at prefrontal cortex were evaluated 24 h after MCAO, and western blot and intracellular calcium were also researched, respectively. Results. RQKL of all doses can improve neurological function and decrease brain infarction, and it performed significant effect in 0, 1.5, 3, and 6 h groups. Moreover, RQKL was able to reduce apoptotic process by reduction of caspase-3 expression, or restraint of eIF2a phosphorylation and caspase-12 activation. It was also able to reduce ROS and modulate intracellular calcium in the brain. Conclusion. RQKL can prevent ischemic-induced brain injury with a time window of 6 h, and its mechanism might be related to suppress ER stress-mediated apoptotic signaling.
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页数:12
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