时珍国医国药
時珍國醫國藥
시진국의국약
LISHIZHEN MEDICINE AND MATERIA MEDICA RESEARCH
2010年
2期
392-394
,共3页
丹参酮%D-半乳糖%β-淀粉样肽蛋白%诱导型一氧化氮合酶%乙酰胆碱酯酶%大鼠
丹參酮%D-半乳糖%β-澱粉樣肽蛋白%誘導型一氧化氮閤酶%乙酰膽堿酯酶%大鼠
단삼동%D-반유당%β-정분양태단백%유도형일양화담합매%을선담감지매%대서
Tanshinone%D-galactose%β-amyloid peptide protein (Aβ)%Inducible nitric oxide synthase(iNOS)%Acetylcholinesterase(AChE)%Rats
目的 探讨丹参酮对D-半乳糖- Aβ_(1-40)致复合痴呆模型大鼠海马内诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)和乙酰胆碱酯酶(acetylcholinesterase,AChE)表达的影响.方法 ① 实验动物随机分成3组:AD模型组:采用1.25% D-半乳糖腹腔注射致衰老结合双侧海马齿状回背侧微量注射凝聚态Aβ_(1-40)复合造模方法,拟建立AD样学习记忆功能障碍的痴呆动物模型;丹参酮治疗组:AD大鼠造模24 h后给予丹参酮[50 mg/(kg·d)];溶媒对照组:与AD大鼠同法注射等量生理盐水.② 采用免疫组织化学和酶组织化学方法,分别观察大鼠海马内iNOS和AChE表达的变化.结果 ①模型组AChE阳性纤维受损,光密度下降(含阳性面积百分比和光密度);iNOS-ir细胞数显著升高,平均光密度增强;与对照组比较差异极显著(P<0.01).②丹参酮处理后,iNOS-ir细胞数明显减少,光密度也下降;AChE阳性神经纤维密度增强;与模型组比较差异有显著性意义(P<0.01).结论 丹参酮改善D-半乳糖- Aβ_(1-40)致复合痴呆大鼠学习记忆障碍的作用机制,可能与保护脑内胆碱能神经,以及降低海马内iNOS的表达有关.
目的 探討丹參酮對D-半乳糖- Aβ_(1-40)緻複閤癡呆模型大鼠海馬內誘導型一氧化氮閤酶(inducible nitric oxide synthase,iNOS)和乙酰膽堿酯酶(acetylcholinesterase,AChE)錶達的影響.方法 ① 實驗動物隨機分成3組:AD模型組:採用1.25% D-半乳糖腹腔註射緻衰老結閤雙側海馬齒狀迴揹側微量註射凝聚態Aβ_(1-40)複閤造模方法,擬建立AD樣學習記憶功能障礙的癡呆動物模型;丹參酮治療組:AD大鼠造模24 h後給予丹參酮[50 mg/(kg·d)];溶媒對照組:與AD大鼠同法註射等量生理鹽水.② 採用免疫組織化學和酶組織化學方法,分彆觀察大鼠海馬內iNOS和AChE錶達的變化.結果 ①模型組AChE暘性纖維受損,光密度下降(含暘性麵積百分比和光密度);iNOS-ir細胞數顯著升高,平均光密度增彊;與對照組比較差異極顯著(P<0.01).②丹參酮處理後,iNOS-ir細胞數明顯減少,光密度也下降;AChE暘性神經纖維密度增彊;與模型組比較差異有顯著性意義(P<0.01).結論 丹參酮改善D-半乳糖- Aβ_(1-40)緻複閤癡呆大鼠學習記憶障礙的作用機製,可能與保護腦內膽堿能神經,以及降低海馬內iNOS的錶達有關.
목적 탐토단삼동대D-반유당- Aβ_(1-40)치복합치태모형대서해마내유도형일양화담합매(inducible nitric oxide synthase,iNOS)화을선담감지매(acetylcholinesterase,AChE)표체적영향.방법 ① 실험동물수궤분성3조:AD모형조:채용1.25% D-반유당복강주사치쇠로결합쌍측해마치상회배측미량주사응취태Aβ_(1-40)복합조모방법,의건립AD양학습기억공능장애적치태동물모형;단삼동치료조:AD대서조모24 h후급여단삼동[50 mg/(kg·d)];용매대조조:여AD대서동법주사등량생리염수.② 채용면역조직화학화매조직화학방법,분별관찰대서해마내iNOS화AChE표체적변화.결과 ①모형조AChE양성섬유수손,광밀도하강(함양성면적백분비화광밀도);iNOS-ir세포수현저승고,평균광밀도증강;여대조조비교차이겁현저(P<0.01).②단삼동처리후,iNOS-ir세포수명현감소,광밀도야하강;AChE양성신경섬유밀도증강;여모형조비교차이유현저성의의(P<0.01).결론 단삼동개선D-반유당- Aβ_(1-40)치복합치태대서학습기억장애적작용궤제,가능여보호뇌내담감능신경,이급강저해마내iNOS적표체유관.
Objective To investigate the effect of tanshinone on levels of iNOS and AChE in hippocampus of dementia model rats induced by D-galactose combination with Aβ_(1-40).Methods ①The experimental animals were randomly divided into three groups. In AD model group 1.25%D-galactose in combination with microinjection of 10 μg incubated amyloid β-peptide 1-40 (Aβ_(1-40)) into the dorsal blade of the dentale gyrus in the hippocampus of rat. In tanshinone therapeutic group,after establishment of rat AD model for 24 h , tanshinone[50 mg/(kg·d)]was given for 14 days by gastric perfusion. In solvent control group,the rats were treated with the same method as AD rats but received injection of the same physiological saline. ② The expression of iNOS and AChE in rat hippocampus were respectively observed by immunohistochemical and histochemical methods .Results ①AChE positive nervous fibers, optical density of AChE positive nervous fibers of AD rats in the hippocampus were decreased.iNOS-ir cells count and the average optical density of AD rats in the hippocampus were significantly increased as compared with solvent control group. ②After tanshinone treatment, iNOS -ir cell count and the optical density were obviously decreased, optical density of AChE-positive nervous fibers were significantly increased as compared with AD model group.Conclusion Mechanism of tanshinone to improve learning and memory impairment in dementia model rats induced by D-galactose in combination with Aβ_(1-40) might be related to protection of cholinergic nerves in brain and decrease of iNOS expression in hippocampus .