中国实用神经疾病杂志
中國實用神經疾病雜誌
중국실용신경질병잡지
CHINESE JOURNAL OF PRACTICAL NERVOUS DISEASES
2014年
19期
10-11
,共2页
Syn%Bax%Bcl-2%帕金森病%结肠
Syn%Bax%Bcl-2%帕金森病%結腸
Syn%Bax%Bcl-2%파금삼병%결장
Syn%Bax%Bcl-2%Parkinson's disease%Colon
目的:检测Syn、Bax、Bcl-2蛋白在帕金森病大鼠模型结肠中的表达及意义,探讨帕金森病消化系统功能紊乱的可能机制。方法采用羟多巴胺(6-hydroxydopamine ,6-O HDA )损毁大鼠中枢黑质多巴胺能神经元,诱导制备实验性帕金森病大鼠模型。应用免疫组化法S-P法检测Syn、Bax、Bcl-2在帕金森病模型大鼠及正常对照组大鼠结肠组织中的表达情况。结果造模成功后,用免疫组化法S-P法,发现帕金森模型大鼠结肠中的Syn和 Bax表达水平较对照组增加,而Bcl-2表达水平较对照组减少。结论帕金森大鼠结肠组织中的Syn及Bax表达增加,Bcl-2表达减少,为研究帕金森患者肠道功能紊乱的机制提供线索。
目的:檢測Syn、Bax、Bcl-2蛋白在帕金森病大鼠模型結腸中的錶達及意義,探討帕金森病消化繫統功能紊亂的可能機製。方法採用羥多巴胺(6-hydroxydopamine ,6-O HDA )損燬大鼠中樞黑質多巴胺能神經元,誘導製備實驗性帕金森病大鼠模型。應用免疫組化法S-P法檢測Syn、Bax、Bcl-2在帕金森病模型大鼠及正常對照組大鼠結腸組織中的錶達情況。結果造模成功後,用免疫組化法S-P法,髮現帕金森模型大鼠結腸中的Syn和 Bax錶達水平較對照組增加,而Bcl-2錶達水平較對照組減少。結論帕金森大鼠結腸組織中的Syn及Bax錶達增加,Bcl-2錶達減少,為研究帕金森患者腸道功能紊亂的機製提供線索。
목적:검측Syn、Bax、Bcl-2단백재파금삼병대서모형결장중적표체급의의,탐토파금삼병소화계통공능문란적가능궤제。방법채용간다파알(6-hydroxydopamine ,6-O HDA )손훼대서중추흑질다파알능신경원,유도제비실험성파금삼병대서모형。응용면역조화법S-P법검측Syn、Bax、Bcl-2재파금삼병모형대서급정상대조조대서결장조직중적표체정황。결과조모성공후,용면역조화법S-P법,발현파금삼모형대서결장중적Syn화 Bax표체수평교대조조증가,이Bcl-2표체수평교대조조감소。결론파금삼대서결장조직중적Syn급Bax표체증가,Bcl-2표체감소,위연구파금삼환자장도공능문란적궤제제공선색。
Objective To detect the expression and significance of Syn ,Bax ,Bcl-2 in colon of rat model of Parkinson's dis-ease ,and to explore the possible mechanism of digestive system disorder of Parkinson's disease. Methods 6-hydroxydopamine (6-OHDA) damaged rat central dopaminergic neurons in the substantia nigra were used to prepare experimental rat model of Parkinson's disease.S-P method of immunohistochemical was applied to detect the expression of Syn ,Bax ,Bcl-2 of rats'colon tissue in rat model of Parkinson's disease and normal control group.Results After the success of the model ,compared with the control group ,Syn and Bax expression levels increased in colon of rat model of Parkinson's disease by immunohistochemical S-P method ,while the Bcl-2 expression level was reduced.Conclusion The expressions of Syn and Bax in colon tissue of rat model of Parkinson's disease increase ,but the expression of Bcl-2 reduces ,which provide clues to research the mechanism of intestinal dysfunction in Parkinson's disease.