中国老年学杂志
中國老年學雜誌
중국노년학잡지
Chinese Journal of Gerontology
2015年
17期
4743-4746
,共4页
蛇床子素%糖尿病脑病%神经保护%炎症%PI3K%Akt%caspase-3
蛇床子素%糖尿病腦病%神經保護%炎癥%PI3K%Akt%caspase-3
사상자소%당뇨병뇌병%신경보호%염증%PI3K%Akt%caspase-3
Osthole%Diabetes-associated cognitive decline%Neuroprotection%Inflammation%PI3K%Akt%caspase-3
目的 探讨蛇床子素( OST)对糖尿病脑病的神经保护作用及其分子机制. 方法 应用水迷宫实验检测OST对糖尿病大鼠模型学习记忆的影响;应用试剂盒法检测不同实验组海马中胆碱酯酶(AChE)和胆碱乙酰基转移酶(ChAT)、炎症因子(包括 NF-κB p65、TNF-α和 IL-1β)和caspase-3的活性;应用Western印迹方法检测检测不同实验组海马中磷酸化Akt( p-Akt)蛋白的表达. 结果 OST改善了糖尿病大鼠模型的学习记忆能力,降低了糖尿病大鼠模型组海马中AChE和炎症因子(包括NF-κB p65、TNF-α和IL-1β)及cascapse-3的活性(P<0.01),提高了ChAT的活性(P<0.01),降低了p-Akt蛋白的表达(P<0.01). 同时,当使用LY294002阻断PI3K后,OST抑制炎症的作用更为明显,且进一步下调了 p-Akt蛋白的表达. 结论 OST对糖尿病脑病大鼠模型具有神经保护作用,这种保护作用可能是通过抑制PI3K/Akt信号通路减轻炎症反应来实现的,其可能成为临床上缓解糖尿病患者并发学习记忆障碍的新型治疗药物.
目的 探討蛇床子素( OST)對糖尿病腦病的神經保護作用及其分子機製. 方法 應用水迷宮實驗檢測OST對糖尿病大鼠模型學習記憶的影響;應用試劑盒法檢測不同實驗組海馬中膽堿酯酶(AChE)和膽堿乙酰基轉移酶(ChAT)、炎癥因子(包括 NF-κB p65、TNF-α和 IL-1β)和caspase-3的活性;應用Western印跡方法檢測檢測不同實驗組海馬中燐痠化Akt( p-Akt)蛋白的錶達. 結果 OST改善瞭糖尿病大鼠模型的學習記憶能力,降低瞭糖尿病大鼠模型組海馬中AChE和炎癥因子(包括NF-κB p65、TNF-α和IL-1β)及cascapse-3的活性(P<0.01),提高瞭ChAT的活性(P<0.01),降低瞭p-Akt蛋白的錶達(P<0.01). 同時,噹使用LY294002阻斷PI3K後,OST抑製炎癥的作用更為明顯,且進一步下調瞭 p-Akt蛋白的錶達. 結論 OST對糖尿病腦病大鼠模型具有神經保護作用,這種保護作用可能是通過抑製PI3K/Akt信號通路減輕炎癥反應來實現的,其可能成為臨床上緩解糖尿病患者併髮學習記憶障礙的新型治療藥物.
목적 탐토사상자소( OST)대당뇨병뇌병적신경보호작용급기분자궤제. 방법 응용수미궁실험검측OST대당뇨병대서모형학습기억적영향;응용시제합법검측불동실험조해마중담감지매(AChE)화담감을선기전이매(ChAT)、염증인자(포괄 NF-κB p65、TNF-α화 IL-1β)화caspase-3적활성;응용Western인적방법검측검측불동실험조해마중린산화Akt( p-Akt)단백적표체. 결과 OST개선료당뇨병대서모형적학습기억능력,강저료당뇨병대서모형조해마중AChE화염증인자(포괄NF-κB p65、TNF-α화IL-1β)급cascapse-3적활성(P<0.01),제고료ChAT적활성(P<0.01),강저료p-Akt단백적표체(P<0.01). 동시,당사용LY294002조단PI3K후,OST억제염증적작용경위명현,차진일보하조료 p-Akt단백적표체. 결론 OST대당뇨병뇌병대서모형구유신경보호작용,저충보호작용가능시통과억제PI3K/Akt신호통로감경염증반응래실현적,기가능성위림상상완해당뇨병환자병발학습기억장애적신형치료약물.
Objective To explore the neuroprotective effects of osthole in rats with diabetes-associated cognitive decline ( DACD) and potential molecular mechanisms.Methods The learning and memory performance were assessed by Morris water maze test;The activi-ties of AChE, ChAT, inflammatory cytokines including NF-κB p65, TNF-αand IL-1βand caspase-3 in the hippocampus were detected by respective commercial kits;Western blot analysis was employed to determine the protein level of phosphor-Akt ( p-Akt) in the hippocampus. Results Osthole significantly improved learning and memory functions in diabetic groups.Additionally, the activities of AChE and inflam-matory cytokines including NF-κB p65, TNF-αand IL-1βand caspase-3 in the hippocampus were all remarkably decreased, while increased ChAT was found in diabetic rats.Furthermore, osthole also diminished the protein expression of p-Akt in diabetic rats.Conclusions Ost-hole exerts protective potential against DACD and this neuroprotection is associated with suppressing PI3K/Akt-mediated inflammation in dia-betic rats.It is likely to be a novel therapeutic drug for the treatment of diabetic patients with cognitive deficits in clinical practice.
