中国药理学通报
中國藥理學通報
중국약이학통보
CHINESE PHARMACOLOGICAL BULLETIN
2014年
11期
1539-1542,1543
,共5页
吴洁%吴红海%于洋%秦亚彬%韩晓磊%侯艳宁
吳潔%吳紅海%于洋%秦亞彬%韓曉磊%侯豔寧
오길%오홍해%우양%진아빈%한효뢰%후염저
阿尔采末病%β-淀粉样蛋白%星形胶质细胞%神经元%孕酮%TNF-α%IL-1β%NF-κB
阿爾採末病%β-澱粉樣蛋白%星形膠質細胞%神經元%孕酮%TNF-α%IL-1β%NF-κB
아이채말병%β-정분양단백%성형효질세포%신경원%잉동%TNF-α%IL-1β%NF-κB
Alzheimer ’ s disease%β-amyloid%astro-cytes%neurons%progesterone%TNF-α%IL-1β%NF-κB
目的：探究孕酮抑制Aβ诱导的星形胶质细胞活化,发挥神经元保护作用及其机制,为孕酮在阿尔采末病( Alzheimer’ s disease, AD)防治中的应用提供实验依据。方法将原代培养的星形胶质细胞随机分为对照组、Aβ组及Aβ加3个浓度孕酮组,分别处理24 h后,与神经元共培养。MTT法检测神经元的存活率；ELISA检测条件培养液中炎症因子IL-1β和TNF-α的水平；免疫荧光法和Western blot检测星形胶质细胞NF-κB的活性。结果孕酮浓度依赖地抑制Aβ诱导的星形胶质细胞活化引起的神经元存活率下降；抑制Aβ诱导的星形胶质细胞IL-1β和TNF-α释放的升高；抑制Aβ诱导星形胶质细胞NF-κB的活性增加。结论孕酮通过抑制Aβ诱导的星形胶质细胞活化,发挥神经元保护作用,其作用机制可能与NF-κB信号通路有关。
目的：探究孕酮抑製Aβ誘導的星形膠質細胞活化,髮揮神經元保護作用及其機製,為孕酮在阿爾採末病( Alzheimer’ s disease, AD)防治中的應用提供實驗依據。方法將原代培養的星形膠質細胞隨機分為對照組、Aβ組及Aβ加3箇濃度孕酮組,分彆處理24 h後,與神經元共培養。MTT法檢測神經元的存活率；ELISA檢測條件培養液中炎癥因子IL-1β和TNF-α的水平；免疫熒光法和Western blot檢測星形膠質細胞NF-κB的活性。結果孕酮濃度依賴地抑製Aβ誘導的星形膠質細胞活化引起的神經元存活率下降；抑製Aβ誘導的星形膠質細胞IL-1β和TNF-α釋放的升高；抑製Aβ誘導星形膠質細胞NF-κB的活性增加。結論孕酮通過抑製Aβ誘導的星形膠質細胞活化,髮揮神經元保護作用,其作用機製可能與NF-κB信號通路有關。
목적：탐구잉동억제Aβ유도적성형효질세포활화,발휘신경원보호작용급기궤제,위잉동재아이채말병( Alzheimer’ s disease, AD)방치중적응용제공실험의거。방법장원대배양적성형효질세포수궤분위대조조、Aβ조급Aβ가3개농도잉동조,분별처리24 h후,여신경원공배양。MTT법검측신경원적존활솔；ELISA검측조건배양액중염증인자IL-1β화TNF-α적수평；면역형광법화Western blot검측성형효질세포NF-κB적활성。결과잉동농도의뢰지억제Aβ유도적성형효질세포활화인기적신경원존활솔하강；억제Aβ유도적성형효질세포IL-1β화TNF-α석방적승고；억제Aβ유도성형효질세포NF-κB적활성증가。결론잉동통과억제Aβ유도적성형효질세포활화,발휘신경원보호작용,기작용궤제가능여NF-κB신호통로유관。
Aim To investigate the effect of progester-one ( PROG) in protecting the neurons against impair-ment induced by the Aβ1-42 activated astrocytes, and the underlying molecular mechanism. Methods The astrocytes were divided into 5 groups: control, Aβ, and Aβplus PROG groups treated with 3 different con-centrations of progesterone for 24h. Then, Aβand pro-gesterone were removed, and neurons were co-cultured with the treated astrocytes. MTT assay was used to e-valuate the viability of cultured neurons; ELISA was used to detect the levels of IL-1βand TNF-αin culture media of astrocytes; immunofluorescence and Western blot were performed to detect the activation of NF-κB in astrocytes. Results PROG dose dependently pro-tected against Aβ1-42 activated astrocytes induced via-bility decrease in co-cultured neurons. Aβ induced release of IL-1β and TNF-α from astrocytes, and in-crease of NF-κB activity was abolished by progesterone treatment. Conclusion PROG protects the neurons through inhibiting the reactivity of astrocytes, and the underlying mechanism involves the NF-κB signal trans-duction.
