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caspase-3 by enhancing Aktl 期刊论文

编号：

79d35364-0867-49c1-9c00-57fc14730b1f
作者：

Qi, DaShi^[1,2,5];Tao, Jinhao^[9];Zhang, LianQin^[1,2,5];Li, Man^[1,2,5];Wang, Mei^[5];Qu, Rui^[6];Zhang, ShiChun^[10];Liu, Pei^[5];Liu, Fuming^[5];Miu, JianCheng^[7];Ma, JingYi^[8];Mei, XinYu^[3,4];Zhang, Fayong(张法永)*^[11]
语种：

English
期刊：

BRAIN RESEARCH ISSN：0006-8993 2016 年 1653 卷 (67 - 74) ; DEC 15
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关键词：

Cilostazol Global cerebral ischemia Rat Cognitive deficits JNK3 Akt1
摘要：

Cilostazol(CTL) is a phosphodiesterase inhibitor, which has been widely used as anti-platelet agent. It also has preventive effects on various central nervous system (CNS) diseases, including ischemic stroke, Parkinson's disease and Alzheimer disease. However, the molecular mechanism underlying the protective effects of CTL is still unclear, and whether CTL can prevent I/R induced cognitive deficit has not been reported. Transient global brain ischemia was induced by 4-vessel occlusion in adult male Sprague-Dawley rats. The open field tasks and Morris water maze were used to assess the effect of CTL on anxiety-like behavioral and cognitive impairment after I/R. Western blotting were performed to examine the expression of related proteins, and HE-staining was used to detect the percentage of neuronal death in the hippocampal CAl region. Here we found that CTL significantly improved cognitive deficits and the behavior of rats in Morris water maze and open field tasks (P < 0.05). HE staining results showed that CTL could significantly protect CAl neurons against cerebral I/R (P < 0.05). Additionally, Aktl phosphorylation levels were evidently up-regulated (P < 0.05), while the activation of JNK3, which is an important contributor to I/R-induced neuron apoptosis, was reduced by CTL after I/R (P < 0.05), and caspase-3 levels were also decreased by CTL treatment. Furthermore, all of CTL's protective effects were reversed by LY294002, which is a PI3K/Aktl inhibitor. Taken together, our results suggest that CTL could protect hippocampal neurons and ameliorate the impairment of learning/memory abilities and locomotor/exploratory activities in ischemic stroke via a PI3K-Aktl/JNK3/caspase-3 dependent mechanism.
推荐引用方式
GB/T 7714：

Qi Da-Shi,Tao Jin-hao,Zhang Lian-Qin, et al. Neuroprotection of Cilostazol against ischemia/reperfusion-induced cognitive deficits through inhibiting JNK3/caspase-3 by enhancing Aktl [J].BRAIN RESEARCH,2016,1653:67-74.
APA：

Qi Da-Shi,Tao Jin-hao,Zhang Lian-Qin,Li Man,&Zhang Fayong.(2016).Neuroprotection of Cilostazol against ischemia/reperfusion-induced cognitive deficits through inhibiting JNK3/caspase-3 by enhancing Aktl .BRAIN RESEARCH,1653:67-74.
MLA：

Qi Da-Shi, et al. "Neuroprotection of Cilostazol against ischemia/reperfusion-induced cognitive deficits through inhibiting JNK3/caspase-3 by enhancing Aktl" .BRAIN RESEARCH 1653(2016):67-74.

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