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Protective Effects and Mechanisms of JHS on Cerebral Ischemia-Reperfusion Injury

Author: ZhangYunLing
Tutor: LiWeiPing；LiWeiZu
School: Anhui Medical University,
Course: Pharmacology
Keywords: cerebral ischemia-reperfusion injury free radical hippocampal neuron cell apoptosis calcium overload Caspase-3
CLC: R743
Type: Master's thesis
Year: 2008
Downloads: 56
Quote: 0
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Abstract


Objective To study the protective effects and mechanisms of JHS on cerebral ischemia-reperfusion injury .Methods1. The experiments of quick decapitation and anoxia under normal pressure model in mice were used to study the effects of JHS on acute cerebral ischemia and anoxia.2. The focal cerebral ischemia-reperfusion model was built by the suture method for middle cerebral artery occlusion (MCAO) in rats. The model was made to observe the effects of JHS on neurological function score, infarction volume of the brain, thrombogenesis in vitro, platelet aggregation, water content and cerebral index; To investigate the activity of SOD, LDH, NOS and the content of MDA, LD in brain tissue; TNF-αand Caspase-3 were observed by immunohistochemistry and brain pathology was studied with morphological method.3. The effects of JHS on cerebral blood flow(CBF), cerebral vascular resistance(CVR) were observed by Ultrasonic Doppler Instrument, blood pressure and heart rate were detected in anaesthesia-rabbit by BL-420E system.4. An anoxia-reoxygenation injured model was established by using primary cultured hippocampal neurons in vitro, the model was made to observe the effects of JHS on activity, the level of apoptosis and the intracellular calcium concentration of hippocampal neuron . Results1. JHS could prolong the gasping time of mice after quick decapitation and survival time of anoxic mice.2. Compared with model group, JHS could decrease the neurological function score after focal cerebral ischemia reperfusion at 8h and 22h; JHS could decrease the infarction volume of brain , the length , wet weight, dry weight of thromb and inhibit platelet aggregation in rats after focal cerebral ischemia reperfusion; JHS could reduce the brain edema, brain index and obviously relieve histopathologic injury in brain tissue; The activity of SOD, LDH of brain were increased, while MDA, LD, NOS decreased after treated by JHS; the expression of TNF-αand Caspase-3 could be inhibited by JHS on focal cerebral ischemia-reperfusion rats.3. JHS could increase the cerebral blood flow and decrease the cerebral vascular resistance in anaesthesia rabbits . There is no obviouse influence on blood pressure after administration of JHS.4. JHS could significantly improve neuronal viability after anoxia-reoxygenation injury of hippocampal neurons, inhibit the apoptosis of the neurons and decrease the intracellular calcium concentration of hippocampal neuron.Conclusion JHS took protective effects on cerebral ischemia-reperfusion injuries. The role of thrombolysis, antioxidation, calcium antagonism, inhibition of platelet aggregation and apoptosis, inhibition the expression of TNF-αand Caspase-3 might contribute to its neuro protective effect.

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