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作 者:Hongxia Xing Hai Peng Xuebing Cao Shenggang Sun
机构地区:[1]Department of Neurology, The First Hospital of Xinxiang Medical College, Xinxiang 453100, Henan Province, China [2]Department of Neurology, Xiehe Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, Hubei Province, China
出 处:《Journal of Nanjing Medical University》2008年第1期12-17,共6页南京医科大学学报(英文版)
基 金:National Natural Sciences Foundation of China(No.30300114)
摘 要:Objective: To study the effects and mechanism of homocysteine(Hcy) on Parkinson' s disease(PD) induced by 6-hydroxydopamine (6-OHDA) in vivo. Methods:Forty rats were divided into 4 groups. 6-OHDA or the solvent of 6-OHDA was focally administrated to induce PD, 2 h later Hcy or 0.9% sodium chloride was administrated in the ipsolateral substantial nigra(SN). We Used behavioral testing, Immolunohistochemical techniques, biochemistry techniques to detect the injury of SN. Results:The rotary turns of PD rats induced by 6-OHDA showed significant increase after treatment with Hcy compared with the controls(P 〈 0.05). Also the numbers of tyrosine hydroxylase(TH)-stained neurons were decreased, and dendrites were fragmented and truncated. Free radicals were increased and antioxidaat enzymes decreased. Conclusion:Focal infusion of Hcy into the SN increased the vulnerability of the doparninergic neurons to 6-OHDA-induced degeneration, it seems that the endangering effect of Hcy is due to exacerbating oxidative stress.Objective: To study the effects and mechanism of homocysteine(Hcy) on Parkinson' s disease(PD) induced by 6-hydroxydopamine (6-OHDA) in vivo. Methods:Forty rats were divided into 4 groups. 6-OHDA or the solvent of 6-OHDA was focally administrated to induce PD, 2 h later Hcy or 0.9% sodium chloride was administrated in the ipsolateral substantial nigra(SN). We Used behavioral testing, Immolunohistochemical techniques, biochemistry techniques to detect the injury of SN. Results:The rotary turns of PD rats induced by 6-OHDA showed significant increase after treatment with Hcy compared with the controls(P 〈 0.05). Also the numbers of tyrosine hydroxylase(TH)-stained neurons were decreased, and dendrites were fragmented and truncated. Free radicals were increased and antioxidaat enzymes decreased. Conclusion:Focal infusion of Hcy into the SN increased the vulnerability of the doparninergic neurons to 6-OHDA-induced degeneration, it seems that the endangering effect of Hcy is due to exacerbating oxidative stress.
关 键 词:Parkinson's disease 6-HYDROXYDOPAMINE HOMOCYSTEINE tyrosine hydroxylase
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