Effects of polysaccharides of the Euphoria Longan (Lour.) Steud on focal cerebral ischemia/reperfusion injury and its underlying mechanism

被引:18
作者
Chen, Jian [2 ]
Chen, Xu [1 ]
Qin, Jian [3 ]
机构
[1] Guilin Med Univ, Sch Pharmaceut, Guilin 541004, Peoples R China
[2] Guilin Med Univ, Dept Physiol, Guilin 541004, Peoples R China
[3] Hosp Guangxi Zhuang Autonomous Reg, Ctr Clin Canc, Dept Radiat Oncol, Nanning, Guangxi, Peoples R China
关键词
Polysaccharides of the Euphoria Longan (Lour.) Steud; cerebral ischemia-reperfusion; oxidative stress; inflammatory response; apoptosis; ISCHEMIA-REPERFUSION INJURY; OXIDATIVE STRESS; RAT-BRAIN; APOPTOSIS; CYTOKINES; NIMODIPINE; PROTECTS;
D O I
10.3109/02699052.2010.546824
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Objective: To investigate the effects of polysaccharides of the Euphoria Longan (Lour.) Steud on focal cerebral ischemia/reperfusion(I/R) injury in rats. Methods: In this study, spectrophotometry was employed to observe the effects of polysaccharides of the Euphoria Longan (Lour.) Steud on O-2(center dot-) and center dot OH in vitro. The operation was performed to induce the middle cerebral artery occlusion (MCAO) in rats. The influences of polysaccharides on the neurological function score, the brain water content, the infarct volume, activities of superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GSH-Px) and myeloperoxidase (MPO), the contents of malondialdehyde (MDA), the protein levels of Bcl-2 and Bax, the concentration of tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-beta) in brain tissue were measured. Results: Compared with the I/R group, polysaccharides of the Euphoria Longan (Lour.) Steud could obviously reduce the neurological score, the infract volume, the brain water content, MDA content, MPO activity, TNF-alpha and IL-1 beta level, expression of Bax, and increase SOD, GSH, GSH-Px activity and expression of Bcl-2. Conclusion: The data suggest that polysaccharides of the Euphoria Longan (Lour.) Steud are capable of alleviating I/R injury by a mechanism that may involve decreasing oxidative stress.
引用
收藏
页码:292 / 299
页数:8
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