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BACKGROUND:Microglia function as the immune surveyors of the brain under normal physiological conditions.However,microglia become activated in response to brain injuries and immunological stimula-tion.OBJECTIVE:To explore the influence of scorpion venom(SV) heat-resistant protein on frontal cortex and hippocampal microglia cells in a mice model of Parkinson’s disease.DESIGN,TIME AND SETTING:Randomized,controlled,cellular immunity study.The experiment was performed at the Physiology Department Laboratory in Dalian Medical University between June 2005 and July 2008.MATERIALS:Ninety-six healthy,C57Bl/6 mice;1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP) from Sigma,USA;SV heat-resistant protein(Experimental Base Institute in Dalian Medical University).The mice were randomly divided into four groups(n = 24):normal control,negative control,model,and SV heat-resistant protein.METHODS:Mice in the model and SV heat-resistant protein groups were subcutaneously injected with MPTP(20 mg/kg) to model Parkinson’s disease,while the normal control and negative control groups were injected with physiological saline in the neck for 8 successive days.In addition,mice in the model and nor-mal control groups were intraperitoneally injected with physiological saline 2 hours following administration,while SV heat-resistant protein and negative control groups were injected SV heat-resistant protein(0.01 mg/kg).MAIN OUTCOME MEASURES:Immunoreactivity of microglia cells in MPTP-treated mice.RESULTS:Compared with normal control mice,MPTP-treated mice displayed increased OX-42 expression in the brain.However,in the SV heat-resistant protein-treated mice,OX-42 expression was decreased,com-pared to the model group.In the model mouse group,the number of OX-42-positive microglia was increased in the frontal cortex,caudatum,and hippocampal hilus,compared to the normal control mice(P < 0.01).However,in the SV heat-resistant protein-treated mice,the number of OX-42-positive microglia significantly decreased in the frontal cortex,caudatum,and hippocampal hilus,compared to the model group(P < 0.01).CONCLUSION:SV heat-resistant protein inhibited MPTP-induced microglial activation in the mouse fron-tal cortex and hippocampus,resulting in reduced microglial activation in the brain.
BACKGROUND:Microglia function as the immune surveyors of the brain under normal physiological conditions.However,microglia become activated in response to brain injuries and immunological stimula-tion.OBJECTIVE:To explore the influence of scorpion venom(SV) heat-resistant protein on frontal Cortex and hippocampal microglia cells in a mice model of Parkinson’s disease.DESIGN,TIME AND SETTING:Randomized,controlled,cellular immunity study.The experiment was performed at the Physiology Department Laboratory in in the Medical Department of Dalian in June 2005 and July 2008.MATERIALS:Ninety -six healthy,C57Bl/6 mice;1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP) from Sigma,USA;SV heat-resistant protein(Experimental Base Institute in Dalian Medical University).The Mice were randomly divided into four groups (n = 24): normal control, negative control, model, and SV heat-resistant protein.METHODS: Mice in the model and SV heat-resistant protein groups were subcutaneously injected with MPTP (20 mg/ Kg) to Model Parkinson’s disease, while the normal control and negative control groups were injected with physiologic saline in the neck for 8 After days.In addition,mice in the model and nor-mal control groups were intraperitoneally integrated with physical saline 2 hours following administration, while SV heat-resistant protein and negative control groups were injected SV heat-resistant protein(0.01 mg/kg).MAIN OUTCOME MEASURES:Immunoreactivity of microglia cells in MPTP-treated mice.RESULTS:Compared with normal control mice,MPTP-treated mice displayed Increased OX-42 expression in the brain.However,in the SV heat-resistant protein-treated mice,OX-42 expression was decreased,com-pared to the model group.In the model mouse group,the number of OX-42- Positive microglia was increased in the frontal cortex, caudatum, and hippocampal hilus,committed to the normal control mice (P < 0.01).However,in the SV heat-resistant protein-treated mice,the number of OX-42-positive microglia significantlyDecreased in the frontal cortex, caudatum, and hippocampal hilus,committed to the model group (P < 0.01).CONCLUSION:SV heat-resistant protein inhibited MPTP-induced microglial activation in the mouse fron-tal cortex and hippocampus,resulting in reduced microglial Activation in the brain.