中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2014年
3期
311-314
,共4页
康文清%亓珅%张诚%韩晓娟%王璐%张清华%张霄%杜怡峰
康文清%亓珅%張誠%韓曉娟%王璐%張清華%張霄%杜怡峰
강문청%기신%장성%한효연%왕로%장청화%장소%두이봉
阿尔茨海默病%白细胞介素1β%肿瘤坏死因子α
阿爾茨海默病%白細胞介素1β%腫瘤壞死因子α
아이자해묵병%백세포개소1β%종류배사인자α
Alzheime disease%Interleukin-l beta%Tumor necrosis factor-alpha
目的 探讨Aβ1-42寡聚体对小胶质细胞白细胞介素(IL)-1β和肿瘤坏死因子(TNF)-α表达的影响,以及海风藤提取物的干预作用. 方法 将小鼠源小胶质细胞株BV2随机分为3组:空白对照组、Aβ1-42组(给予Aβ142寡聚体)、Aβ1-42+海风藤提取物组(在给予Aβ1-42寡聚体的基础上加用海风藤提取物干预).按实验要求作用48 h后,实时荧光定量聚合酶链反应(RT-PCR)方法检测各组细胞IL-1β、TNF-α mRNA含量,蛋白印迹法(Western blot)检测各组细胞IL-1β、TNF-α蛋白表达量. 结果 Aβ1-42寡聚体组IL-1β、TNF-α mRNA表达量分别为对照组的(21.9±0.4)倍、(3.8±0.3)倍,较对照组显著升高(t=88.67、16.47,均P=0.000);Aβ1-42寡聚体+海风藤提取物组IL1β、TNF-α mRNA表达量分别为对照组的(8.3±0.3)倍、(1.3±0.2)倍,但较Aβ1-42寡聚体组明显下降(t=57.70、14.71,均P=0.000).Aβ1-42寡聚体组IL-1β、TNF-α蛋白表达量分别为83.3±8.5、32.0±3.6,较空白对照组25.2±13.9、2.6±1.7明显增加(t=7.46、11.74,均P=0.000);Aβ1-42寡聚体+海风藤提取物组IL-1β、TNF-α蛋白表达量分别为59.3±2.7、21.7±4.5,较Aβ1-42寡聚体组明显减少(t=3.08、4.38,P=0.022、0.005). 结论 海风藤提取物可以明显抑制Aβ1-42寡聚体激活小胶质细胞引起的IL-1β、TNF-α mRNA及蛋白的过量表达.
目的 探討Aβ1-42寡聚體對小膠質細胞白細胞介素(IL)-1β和腫瘤壞死因子(TNF)-α錶達的影響,以及海風籐提取物的榦預作用. 方法 將小鼠源小膠質細胞株BV2隨機分為3組:空白對照組、Aβ1-42組(給予Aβ142寡聚體)、Aβ1-42+海風籐提取物組(在給予Aβ1-42寡聚體的基礎上加用海風籐提取物榦預).按實驗要求作用48 h後,實時熒光定量聚閤酶鏈反應(RT-PCR)方法檢測各組細胞IL-1β、TNF-α mRNA含量,蛋白印跡法(Western blot)檢測各組細胞IL-1β、TNF-α蛋白錶達量. 結果 Aβ1-42寡聚體組IL-1β、TNF-α mRNA錶達量分彆為對照組的(21.9±0.4)倍、(3.8±0.3)倍,較對照組顯著升高(t=88.67、16.47,均P=0.000);Aβ1-42寡聚體+海風籐提取物組IL1β、TNF-α mRNA錶達量分彆為對照組的(8.3±0.3)倍、(1.3±0.2)倍,但較Aβ1-42寡聚體組明顯下降(t=57.70、14.71,均P=0.000).Aβ1-42寡聚體組IL-1β、TNF-α蛋白錶達量分彆為83.3±8.5、32.0±3.6,較空白對照組25.2±13.9、2.6±1.7明顯增加(t=7.46、11.74,均P=0.000);Aβ1-42寡聚體+海風籐提取物組IL-1β、TNF-α蛋白錶達量分彆為59.3±2.7、21.7±4.5,較Aβ1-42寡聚體組明顯減少(t=3.08、4.38,P=0.022、0.005). 結論 海風籐提取物可以明顯抑製Aβ1-42寡聚體激活小膠質細胞引起的IL-1β、TNF-α mRNA及蛋白的過量錶達.
목적 탐토Aβ1-42과취체대소효질세포백세포개소(IL)-1β화종류배사인자(TNF)-α표체적영향,이급해풍등제취물적간예작용. 방법 장소서원소효질세포주BV2수궤분위3조:공백대조조、Aβ1-42조(급여Aβ142과취체)、Aβ1-42+해풍등제취물조(재급여Aβ1-42과취체적기출상가용해풍등제취물간예).안실험요구작용48 h후,실시형광정량취합매련반응(RT-PCR)방법검측각조세포IL-1β、TNF-α mRNA함량,단백인적법(Western blot)검측각조세포IL-1β、TNF-α단백표체량. 결과 Aβ1-42과취체조IL-1β、TNF-α mRNA표체량분별위대조조적(21.9±0.4)배、(3.8±0.3)배,교대조조현저승고(t=88.67、16.47,균P=0.000);Aβ1-42과취체+해풍등제취물조IL1β、TNF-α mRNA표체량분별위대조조적(8.3±0.3)배、(1.3±0.2)배,단교Aβ1-42과취체조명현하강(t=57.70、14.71,균P=0.000).Aβ1-42과취체조IL-1β、TNF-α단백표체량분별위83.3±8.5、32.0±3.6,교공백대조조25.2±13.9、2.6±1.7명현증가(t=7.46、11.74,균P=0.000);Aβ1-42과취체+해풍등제취물조IL-1β、TNF-α단백표체량분별위59.3±2.7、21.7±4.5,교Aβ1-42과취체조명현감소(t=3.08、4.38,P=0.022、0.005). 결론 해풍등제취물가이명현억제Aβ1-42과취체격활소효질세포인기적IL-1β、TNF-α mRNA급단백적과량표체.
Objective To investigate the effect of oligomeric Aβ1-42 on the expressions of interleukin (IL)-lβ and tumor necrosis factor(TNF)-α in microglia cells,and to observe the impact of piper kadsura ohwi extracts induced by oligomeric Aβ1-42.Methods Murine microglial cell line BV2 were randomly divided into 3 groups:control group (without any intervention),oligomericAβ142 group (intervened by oligomeric Aβ1-42),oligomeric Aβ1-42 + piper kadsura ohwi extracts group (intervened by oligomeric Aβ1-42 and piper kadsura ohwi extracts).After 48 hours of the intervention,levels of IL-1β and TNF-α were determined by RT-PCR and Western blotting.Results Compared with the control group,the levels of IL-1β and TNF α mRNA were significantly increased by (21.9± 0.4) folds and (3.8±0.3) folds in oligomeric Aβ1 42 group (t=88.67,16.47,both P<0.001) and by (8.3±0.3) folds and (1.3±0.2) folds in oligomeric A1-42 + Piper kadsura ohwi extracts group (t=30.97,P<0.001; t=1.77,P>0.05).The Aβ1-42 induced expressions of IL-1β and TNF-α mRNA were markedly decreased in oligomeric Aβ1-42+ Piper kadsuraohwi extracts group (t=57.70,14.71,both P<0.001).Western blotting showed that the protein expressions of IL-1β and TNF-α were increased in oligomeric Aβ1-42 group as compared with the control group [(83.3± 8.5) vs.(25.2 ± 13.9),(32.0±3.6)vs.(2.6±1.7),t=7.46,11.74,both P<0.001].The protein expressions of IL-1β and TNF-α were decreased in oligomeric Aβ1 42 + Piper kadsura ohwi extracts group as compared with the oligomeric Aβ1-42 group[(59.3±2.7) vs.(83.3±8.5),(21.7±4.5) vs.(32.0±3.6),t=3.08,4.38,P<0.05 or 0.01].Conclusions Piper kadsura ohwi extracts can inhibit the microglia over-expressions of IL-1β and TNF-α activated by oligomeric Aβ1-42.