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Reasearch of Ginsenoside Rd Promotes Neurogenesis after Cerebral Ischemic Stroke in Adult Rats

Author: ZhaoHaiBo
Tutor: ZhaoGang
School: Fourth Military Medical University
Course: Neurology
Keywords: Ginsenoside Rd Cerebral ischemia Neurogenesis
CLC: R743.33
Type: Master's thesis
Year: 2013
Downloads: 16
Quote: 0
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Despite improvements in its management in recent years, stroke remains a major causeof mortality, morbidity and disability, resulting in impaired movement, poor life qualityand massive economic loss worldwide. The third national survey of the cause of deadpeople in2008, organized by Ministry of Public Health of China, indicated that strokehad became the first leading cause of death in China and the ischemic stroke accounted forabout80%or more of the total stroke. There is in badly need of an effective treatment forischemic stroke. As its complexity of pathogenesis, therapeutic options are hot but difficultfields in clinical research. Currently thrombolytic therapy is the most effective strategyamong multitudinous treatments. However, the short therapeutic window, together withthe extensive exclusion criteria, severely restricts its use.Pharmacological neuroprotective approaches to reduce ischemic brain damage afterstroke have largely failed to translate to the clinic in recent years. Nowdays more andmore studies focus on nuerorepair, which has emerged as a potential therapy for brainischemic at acute and subacute stage of ischemic stroke. As we all known, the brain wo uldrepair itself after stroke without any medical therapy due to activated endogenousneurogenesis. So a method of promoting endogenous neurogenesis to improve outcomesin patients with ischemic stroke will be a promising research.GSRd, a new drug owning absolutely intellectual property pretection, was firstlyconfirmed its neuroprotective effecacy in our randomized, double-blind, placebo-controlled, multicenter trial. And based on the previous animal experiments, GSRd may protect against ischemic injury by anti-oxidative stress, maintaining mitochondrialmembrane potential at the early stage of stroke. Amazingly, GSRd also exertsneuroprotection at subacute stage of stroke, involving that it enhanced proliferation ofneural stem/progenitor cells in the SVZ and SGZ in vivo and induced neural stem cellsdifferentiation into neurons in vitro. We propose that GSRd protects ischemic brainthrough activating neurogenesis at subacute stage of ischemic stroke.Objective:To research the effect of GSRd to neurogenesis in SVZ at different timepoints aftercerebral ischemia stroke by MCAO/R animal model in adult rats.Methods:(1) Male adult SD rats were subjected to transient focal occlusion of the middle cerebralartery/reperfusion (MCAO/R). The sham group is similar to the MCAO/R group exceptnot obstruct the blood supply of MCA.Then assess the stability of animal model by theneurological score and TTC staining.(2)At post-ischemia6h、24h and3d, the ratsreceived GSRd or placebo at doses of10mg/kg/d by the intraperitoneal administration,daily for an additional7d. To investgate the proliferation, migration and differentiation ofNSCs at different timepoints (1w、2w、3w and4w) by immunohistochemistry methods.Results:(1) The method to build MCAO/R model by suture is stable and successful.(2) Compared with control group, GSRd can promote the proliferation and migration ofNSCs significantly at post-ischemia6h and1d, but the effects get weakened graduallywith time delay,the effects of differentiation is not obvious;At post-ischemia3d,GSRd isnot helpful to neurogenesis.Conclusion:GSRd can promote the proliferation of NSCs within24h after cerebral ischemiastroke,but the effects to migration and differentiation are not significant.

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CLC: > Medicine, health > Neurology and psychiatry > Neurology > Cerebrovascular disease > Acute cerebrovascular disease ( stroke) > Cerebral embolism
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