神经保护
自噬
神经炎症
医学
罗格列酮
缺血
冲程(发动机)
海马体
再灌注损伤
药理学
脑缺血
程序性细胞死亡
神经科学
炎症
受体
内科学
生物
细胞凋亡
机械工程
生物化学
工程类
作者
Zi‐Qiang Shao,Zunjing Liu
标识
DOI:10.1016/j.jns.2014.12.027
摘要
Ischemic stroke is one of the leading causes of mortality and disability with documented high incidence and relapse rate. Accumulating evidence indicates that autophagy participated in neuronal cell death and functional loss induced following ischemia/reperfusion (I/R) injury. The peroxisome proliferating activating receptor-γ (PPAR-γ) agonist, Rosiglitazone (RSG), is known for its anti-inflammatory actions. Previous studies have demonstrated that RSG can exert neuroprotection in animal models of both chronic brain injuries and acute brain insults. However, whether RSG treatment is involved in the autophagic neuronal death following I/R injury remains totally unclear. The present study aimed to hypothesize that treatment of RSG could induce neuroprotective properties in a rat model of global cerebral ischemia (GCI), and thereby to investigate the underline mechanisms. We found that a single injection of RSG immediately following GCI significantly reduced cerebral infarct volume and brain edema, as well as increased neuron survival rate and function recovery. These effects correlate with a decrease of inflammatory cytokines and autophagy-associated proteins expression in the hippocampus region. Our results provide in vivo evidence that RSG significantly protected rats against I/R injury induced brain injury, and the mechanism might associate with inhibiting the processes of neuroinflammation and thereby attenuated of neuronal autophagic death. All data suggest that RSG can be further developed as a clinical neuroprotective candidate in ischemic stroke.
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