CAJ | 학술논문

目的研究PET技术评价中药复智散(FZS)治疗自然老化阿尔茨海默病(AD)大鼠疗效的可行性.方法采用中药FZS治疗10只AD大鼠模型30 d后,通过Morris水迷宫测试大鼠行为学改变;另10只AD大鼠以蒸馏水连续30 d灌胃,作为对照组,10只正常成年大鼠作为空白对照组.所有大鼠分别行18F-脱氧葡萄糖(FDG)、2-(4'-N-11C-甲胺基苯)-6-羟基苯并噻唑(PIB)PET脑显像,并取脑组织样本行HE染色、β淀粉样蛋白(Aβ)免疫荧光、5-溴-2-脱氧尿嘧啶核苷(BrdU)免疫荧光和神经元核心抗原(NeuN)免疫荧光染色.采用SPSS 13.0软件对行为学测试结果行配对t检验.结果 FZS治疗后AD大鼠行为学较AD对照组有明显改善,药物治疗组AD大鼠潜伏期[(32.5±10.8)s]明显短于AD对照组[(102.6±8.8)s](t=15.7987,P=0.0001),PET显像显示治疗后AD大鼠脑内葡萄糖代谢有所改善,而淀粉样物质的显像未见明显好转,该结果与病理结果一致.结论 PET显像可作为在体评价AD疗效的一种手段;中药FZS可以通过增加神经细胞的增殖和存活而改善老年大鼠的记忆能力.
목적 연구PET기술평개중약복지산(FZS)치료자연노화아이자해묵병(AD)대서료효적가행성.방법 채용중약FZS치료10지AD대서모형30 d후,통과Morris수미궁측시대서행위학개변;령10지AD대서이증류수련속30 d관위,작위대조조,10지정상성년대서작위공백대조조.소유대서분별행18F-탈양포도당(FDG)、2-(4'-N-11C-갑알기분)-6-간기분병새서(PIB)PET뇌현상,병취뇌조직양본행HE염색、β정분양단백(Aβ)면역형광、5-추-2-탈양뇨밀정핵감(BrdU)면역형광화신경원핵심항원(NeuN)면역형광염색.채용SPSS 13.0연건대행위학측시결과행배대t검험.결과 FZS치료후AD대서행위학교AD대조조유명현개선,약물치료조AD대서잠복기[(32.5±10.8)s]명현단우AD대조조[(102.6±8.8)s](t=15.7987,P=0.0001),PET현상현시치료후AD대서뇌내포도당대사유소개선,이정분양물질적현상미견명현호전,해결과여병리결과일치.결론 PET현상가작위재체평개AD료효적일충수단;중약FZS가이통과증가신경세포적증식화존활이개선노년대서적기억능력.
Objective To assess the feasibility of using PET molecular imaging to evaluate the therapeutic effects of traditional Chinese medicine FuZhiSan (FZS) on the model of aging Alzheimer's disease (AD) rats. Methods Twenty aged AD rats (Sparague-Dawley rats,male) were randomly divided into FZS treated group (n = 10) and control group (n = 10). Another 10 healthy adult rats were as blank controls. Morris water maze record system was used for cognitive function assessment. Before and after FZS treatment 18 F-fluorodeoxyglucose (FDG) and 11 C-2- [4'-(methylamino) phenyl] benzothiazol-6-ol ( PIB )PET imaging was undertaken. After post-treatment imaging procedures the brain tissues of all animals were taken for histochemical study,such as staining with HE,congo red,amyloid β (Aβ) immunofluorescence,5-bromo-2-deoxyuridine (BrdU) immunofluorescence and NeuN immunofluorescence. Paired t-test was performed with SPSS 13.0 software for the data analysis. Results The cognitive dysfunction of aging AD rats was improved after FZS treatment. The escape latency in FZS treated group was significantly shorter than that of control group ((32.5 ±10.8) s vs (102.6±8.8) s,t =15.7987,P=0. 0001). Diffuse neuronal loss and Aβ deposition were detected in the hippocampus and cortex in the aged AD rats. The imaging data showed that brain glucose metabolism was amended in FZS treated group while the abatement of amyloid deposition was not significant. Immunofluorescence results indicated that the neuronal proliferation was more remarkable in FZS treated group. Conclusions It may be feasible to use PET imaging as a method to evaluate the therapeutic effect in AD rats. FZS may ameliorate memory dysfunction of aged AD rats. Its mechanism may be partly contributed to the enhancement of the neuronal proliferation and survival.