中国生化药物杂志
中國生化藥物雜誌
중국생화약물잡지
CHINESE JOURNAL OF BIOCHEMICAL PHARMACEUTICS
2014年
1期
12-15
,共4页
表没食子儿茶素没食子酸酯%APP/PS1转基因小鼠%TNF-α/JNK信号%胰岛素抵抗
錶沒食子兒茶素沒食子痠酯%APP/PS1轉基因小鼠%TNF-α/JNK信號%胰島素牴抗
표몰식자인다소몰식자산지%APP/PS1전기인소서%TNF-α/JNK신호%이도소저항
epigallocatechin-3-gallate%APP/PS 1 transgenetic mice%TNF-α/JNK signaling%insulin resistance
目的：探讨EGCG没食子酸酯（epigallocatechin-3-gallate，EGCG）减轻APP/PS1转基因小鼠海马胰岛素抵抗并改善认知功能机制。方法24只12月龄雌性APP/PS1小鼠随机均分为模型组（Tg）、EGCG低剂量组（Tg/EGCG-L）、高剂量组（Tg/EGCG-H），同月龄雌性C 57 BL/6 J小鼠作为对照组（NT）。采用Morris水迷宫检测各组小鼠学习、记忆能力，Western blot和免疫组织化学方法检测各组小鼠海马TNF-α/JNK信号及IRS-1 pSer 312的表达。结果与NT组比较，Tg组小鼠寻找平台的逃避潜伏期及平均路程显著延长（P＜0.05），海马TNF-α/JNK信号异常活化、IRS-1 pSer 312表达明显升高（P＜0.05）.EGCG各治疗组较Tg组各异常指标均显著改善（P＜0.05）。结论 EGCG可减轻APP/PS1转基因小鼠海马胰岛素抵抗，改善认知功能，其机制可能与其降低TNF-α/JNK信号通路的活化相关。
目的：探討EGCG沒食子痠酯（epigallocatechin-3-gallate，EGCG）減輕APP/PS1轉基因小鼠海馬胰島素牴抗併改善認知功能機製。方法24隻12月齡雌性APP/PS1小鼠隨機均分為模型組（Tg）、EGCG低劑量組（Tg/EGCG-L）、高劑量組（Tg/EGCG-H），同月齡雌性C 57 BL/6 J小鼠作為對照組（NT）。採用Morris水迷宮檢測各組小鼠學習、記憶能力，Western blot和免疫組織化學方法檢測各組小鼠海馬TNF-α/JNK信號及IRS-1 pSer 312的錶達。結果與NT組比較，Tg組小鼠尋找平檯的逃避潛伏期及平均路程顯著延長（P＜0.05），海馬TNF-α/JNK信號異常活化、IRS-1 pSer 312錶達明顯升高（P＜0.05）.EGCG各治療組較Tg組各異常指標均顯著改善（P＜0.05）。結論 EGCG可減輕APP/PS1轉基因小鼠海馬胰島素牴抗，改善認知功能，其機製可能與其降低TNF-α/JNK信號通路的活化相關。
목적：탐토EGCG몰식자산지（epigallocatechin-3-gallate，EGCG）감경APP/PS1전기인소서해마이도소저항병개선인지공능궤제。방법24지12월령자성APP/PS1소서수궤균분위모형조（Tg）、EGCG저제량조（Tg/EGCG-L）、고제량조（Tg/EGCG-H），동월령자성C 57 BL/6 J소서작위대조조（NT）。채용Morris수미궁검측각조소서학습、기억능력，Western blot화면역조직화학방법검측각조소서해마TNF-α/JNK신호급IRS-1 pSer 312적표체。결과여NT조비교，Tg조소서심조평태적도피잠복기급평균로정현저연장（P＜0.05），해마TNF-α/JNK신호이상활화、IRS-1 pSer 312표체명현승고（P＜0.05）.EGCG각치료조교Tg조각이상지표균현저개선（P＜0.05）。결론 EGCG가감경APP/PS1전기인소서해마이도소저항，개선인지공능，기궤제가능여기강저TNF-α/JNK신호통로적활화상관。
Objective To explore mechanism of epigallocatechin-3-gallate (EGCG) on improvement of cognitive function and alleviation of hippocampal insulin resistance in APP/PS 1 transgenetic mice. Method 12 months old female APP/PS 1 mice were randomly divided into 3 groups:model group(Tg), EGCG low dose group (Tg/EGCG-L), high dose group(Tg/EGCG-H). C 57 BL/6 J mice were utilized as control. learning and memory ability in 4 group mice were detected by morris water maze test(MWM). The hippocampal TNF-α/JNK signal and IRS-1 pSer 312 expression were detected by Western blot and immunohistochemical staining. Results Compared with NT mice, Tg mice showed a marked prolongation of the escape latency and swimming distance in the MWM test(P<0.05);Abnormal activation of TNF-α/JNK signaling and increased IRS-1 pSer 312 expression in the hippocampus of Tg mice(P<0.05). EGCG-treated Tg mice showed significantly improvement of all these abnormal changes(P<0.05). Conclusion EGCG treatment is able to alleviate hippocampal insulin resistance and improve cognitive function in the APP/PS 1 mice. which may be partly attributed to the reduction of TNF-α/JNK signaling activity in this AD mouse model.
