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Neuroprotective Effect of Ginsenoside Rd Against Ischemic Neuronal Damage: An in Vitro and in Vivo Study

Author: YeRuiDong
Tutor: ZhaoGang;HanJunLiang
School: Fourth Military Medical University
Course: Neurology
Keywords: Ginsenoside Rd Cerebral ischemia Neuroprotective Oxygen and glucose deprivation
CLC: R285
Type: Master's thesis
Year: 2008
Downloads: 166
Quote: 1
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Stroke is the second leading cause of death in the world, is the second leading cause of loss of labor-adjusted life years in developed countries, and the second cause of death of women in China, male causes of death in the third. Ischemic stroke accounts for about 80% of the stroke, early treatment mainly in two ways: recanalization and neuroprotective treatment. TPA thrombolytic therapy is limited by its overly narrow time window and the fear of bleeding and other complications, not yet widely used. Neuroprotective goal is to save the ischemic penumbra brain tissue still vibrant, Although many neuroprotective drugs failed in clinical trials to prove its validity, but its still hot spots in the early treatment of stroke research, challenging . Ginsenosides The Rd (GSRd) is one of the main active ingredients of ginseng saponins, Notoginseng content of up to 4.07%, and the practical application of the economy. Recent studies show that to antagonize Ca2 channel GSRd kainate and oxidative damage to the central nervous system has a protective effect. In this study, using the hippocampal neurons of oxygen and glucose deprivation (OGD) model and rat brain artery occlusion (MCAO) model, discussed GSRd the neuroprotective effects and possible mechanisms of action. OGD injury model of hippocampal neurons vitro purpose of research GSRd protective effect and the possible mechanism of action. Methods drawn since 18 days gestation fetal rat cells, to cultured neurons B27/Neurobasal medium. Cultured in vitro to the first 6-8 days OGD experiments. OGD for 2 h, after complex sugar reoxygenation 24 h. One set of experiments GSRd before OGD and the OGD end when reoxygenation administered twice delayed therapeutic effect, another set of experiments GSRd only in OGD end, the beginning of reoxygenation administration. After 24 h using LDH method and Hoechst 33342/PI,, double staining to assess cell viability. Show reactive oxygen species (ROS), with a fluorescent dye DCFH-DA with rhodamine 123 mitochondrial membrane potential (MMP). The fluorescence intensity is measured by flow cytometry. Level of malondialdehyde (MDA) and superoxide dismutase (SOD) activity kit for spectrophotometric measurements. We also examined the GSRd against glutamate excitotoxicity protective effect. 2 h of OGD results PI absorption method capable of causing about 50% of cell necrosis, GSRd (0.1-10μM) was able to significantly reduce the number of necrotic cells. The LDH method also come to a similar trend. In Instead, GSRd postponed administration failed to show a significant protective effect. After OGD, ROS increased to 2.08 times the baseline, GSRd can significantly reduce the accumulation of ROS, decreased MDA levels and increased SOD activity. OGD leads to mitochondrial depolarization, performance reduced to a baseline of 40.3% for the fluorescence intensity of rhodamine 123 GSRd stable expression of MMP. Model of excitotoxicity, glutamate led to a large number of LDH leakage, show significant cell damage. The dramatic, GSRd almost completely eliminate this injury. The conclusion GSRd OGD injury has a protective effect in cultured hippocampal neurons, This may be related to inhibition of oxidative stress injury, to maintain MMP and confrontation glutamate toxicity effects. 2 in the rat model of focal cerebral ischemia in vivo purposes further explore GSRd the neuroprotective effect. Focal cerebral ischemia model was prepared with the suture method ischemia duration 2 h reperfusion also to give GSRd or solvent (saline) control treatment. 24 h after the the the neurological deficits check and assess infarct volume by TTC staining. Results after 24 h of reperfusion, solvent treatment group compared GSRd treatment group animals neuroethology showed significant improvement (GSRd 10 mg / Kg, P = 0.012; GSRd 30 mg / kg, P = 0.002) . The average volume of cerebral infarction of the the solvent treatment group animals was 232.7 mm3. GSRd treatment can significantly reduce infarct volume (10 mg / Kg, 189.2 mm3, P = 0.018; of 30 mg / Kg, 178.7 mm3, P = 0.004), 5 mg / Kg treatment group showed borderline statistical significance (200.3 mm3, P = 0.074). Conclusion GSRd (10, 30 mg / Kg) can significantly improve the neurological deficit recovery and reduce infarct volume.

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