【摘 要】
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OBJECTIVE To investigate whether analgesia of oxymatrine relates to high-voltage dependent calcium channels and inhibitory neurotransmitter GABA with neuropathic pain model of mice.METHODS The partial
【机 构】
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Dept of Pharmacol., School of Basic Medical Science, Key Lab of Ministry of Education for TCM Viscer
【出 处】
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The 9th Asian Biophysics Association Symposium (ABA2015)(第九届
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OBJECTIVE To investigate whether analgesia of oxymatrine relates to high-voltage dependent calcium channels and inhibitory neurotransmitter GABA with neuropathic pain model of mice.METHODS The partial sciatic nerve ligation (PSNL) was executed on C57/BL6 mice to produce neuropathic pain.With intraperitoneal administration of oxymatrine (150 mg·kg-1) to PSNL mice, 1) Mechanical hindpaw withdral threshold(MVVT) was measured and ED50 was calculated under Von-Frey filament stimulation with up-and-down method;2) GABA concentration was measured with ELISA method;3) Change of GABAA receptor protein expression, N-type calcium channel (Cav2.2) and L-type calcium channel (Cav1.3) protein expressions were detected with Western-blot.RESULTS 1)Oxymatrine significantly increased ED50 of MVMT on PSNL mice (P＜0.05);2) neuropathic pain condition led to decrease of GABA concentration and GABAA receptor protein level in brain tissue, but administration of oxymatrine reversed this phenomenon and increased both GABA concentration and GABAA receptor expression;3) PSNL-induced significant decrease of Cav2.2 protein expression level was restored by oxymatrine, while Cav1.3 protein expression didnt show any change by either PSNL or oxymatrine treatment.CONCLUSION Analgesia of oxymatrine under neuropathic pain condition is related to the increase of GABA release and GABAA receptor expression, and also the restoration of Cav2.2 protein expression level, which suggests that Cav2.2 calcium channel plays an important role in oxymatrines analgesia.
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