中国中医药信息杂志
中國中醫藥信息雜誌
중국중의약신식잡지
CHINESE JOURNAL OF INFORMATION ON TRADITIONAL CHINESE MEDICINE
2013年
10期
38-40,43
,共4页
朱晶%邵水金%崔国红%田金鑫%陆萍萍%牟芳芳%国海东
硃晶%邵水金%崔國紅%田金鑫%陸萍萍%牟芳芳%國海東
주정%소수금%최국홍%전금흠%륙평평%모방방%국해동
电针血清%神经元%凋亡%β淀粉样蛋白%阿尔茨海默病%大鼠
電針血清%神經元%凋亡%β澱粉樣蛋白%阿爾茨海默病%大鼠
전침혈청%신경원%조망%β정분양단백%아이자해묵병%대서
electro-acupuncture serum%neuron%apoptosis%β-amyloid protein%Alzheimer’s disease%rats
目的观察电针血清对β淀粉样蛋白(Aβ)诱导的原代大鼠海马神经元的保护作用。方法通过Aβ1-40脑内注射建立阿尔茨海默病大鼠模型,予以电针治疗后,留取各组血清。Aβ25-35处理原代培养海马神经元建立体外神经元损伤模型,实验分为正常组、模型组和电针血清组,通过MTT法检测神经元的增殖,采用TUNEL染色法检测神经元的凋亡,通过免疫细胞化学染色检测Caspase-3的表达。结果 MTT检测结果发现,经Aβ处理后,细胞活力显著下降。而与模型组比较,电针血清组细胞增殖能力明显增强(P<0.01);TUNEL 染色结果显示,与模型组比较,电针血清组凋亡细胞数目明显减少(P<0.01);经Aβ处理48 h后,Caspase-3表达水平明显升高,电针血清组Caspase-3阳性细胞数目较模型组显著减少(P<0.01)。结论电针血清能促进海马神经元的增殖,降低其 Caspase-3的表达,对抗Aβ的神经毒性,减少神经元的凋亡。
目的觀察電針血清對β澱粉樣蛋白(Aβ)誘導的原代大鼠海馬神經元的保護作用。方法通過Aβ1-40腦內註射建立阿爾茨海默病大鼠模型,予以電針治療後,留取各組血清。Aβ25-35處理原代培養海馬神經元建立體外神經元損傷模型,實驗分為正常組、模型組和電針血清組,通過MTT法檢測神經元的增殖,採用TUNEL染色法檢測神經元的凋亡,通過免疫細胞化學染色檢測Caspase-3的錶達。結果 MTT檢測結果髮現,經Aβ處理後,細胞活力顯著下降。而與模型組比較,電針血清組細胞增殖能力明顯增彊(P<0.01);TUNEL 染色結果顯示,與模型組比較,電針血清組凋亡細胞數目明顯減少(P<0.01);經Aβ處理48 h後,Caspase-3錶達水平明顯升高,電針血清組Caspase-3暘性細胞數目較模型組顯著減少(P<0.01)。結論電針血清能促進海馬神經元的增殖,降低其 Caspase-3的錶達,對抗Aβ的神經毒性,減少神經元的凋亡。
목적관찰전침혈청대β정분양단백(Aβ)유도적원대대서해마신경원적보호작용。방법통과Aβ1-40뇌내주사건립아이자해묵병대서모형,여이전침치료후,류취각조혈청。Aβ25-35처리원대배양해마신경원건입체외신경원손상모형,실험분위정상조、모형조화전침혈청조,통과MTT법검측신경원적증식,채용TUNEL염색법검측신경원적조망,통과면역세포화학염색검측Caspase-3적표체。결과 MTT검측결과발현,경Aβ처리후,세포활력현저하강。이여모형조비교,전침혈청조세포증식능력명현증강(P<0.01);TUNEL 염색결과현시,여모형조비교,전침혈청조조망세포수목명현감소(P<0.01);경Aβ처리48 h후,Caspase-3표체수평명현승고,전침혈청조Caspase-3양성세포수목교모형조현저감소(P<0.01)。결론전침혈청능촉진해마신경원적증식,강저기 Caspase-3적표체,대항Aβ적신경독성,감소신경원적조망。
Objective To explore the protective effects of electro-acupuncture (EA) serum onβ-amyloid protein (Aβ) induced primary rat hippcampal neurons. Methods The rat models of Alzheimer's disease were established by intracerebral injection of Aβ1-40. After treated them with EA, the serum was harvested. Primary cultured hippocampal neurons were treated with Aβ25-35 to establish neuronal damage model in vitro, and divided into normal group, model group and EA serum group. The proliferation of neurons was detected by MTT test. Neuronal apoptosis was examined by TUNEL staining, and expression of cysteine aspartic acid proteases-3 (Caspase-3) was detected by immunocytochemical staining. Results MTT test showed that the cell viability was significantly decreased after treated with Aβ. While compared with the model group, cell proliferation of EA serum group was significantly enhanced (P<0.01). TUNEL staining showed that the number of apoptotic cells in EA serum group decreased significantly compared with the model group (P<0.01). After 48 h of Aβ treatment, Caspase-3 expression levels were significantly elevated. However, compared with the model group, the number of Caspase-3 positive cells in EA serum group was significantly reduced (P<0.01). Conclusion The EA serum could promote the proliferation of hippocampal neurons, reduce the expression of Caspase-3, counteract the neurotoxicity of β-amyloid protein, and reduce neuronal apoptosis.