摘要
目的:探讨牛蒡子苷元(ARC)调节PI3K/AKT信号通路对创伤后应激障碍(PTSD)模型大鼠认知能力的影响。方法:将大鼠随机分为对照(CK)组、Model组、ARC低剂量(ARC-L)组、ARC高剂量(ARC-H)组、ARC高剂量+LY294002(ARCH+LY294002)组。采用Morris水迷宫检测大鼠空间学习记忆能力;ELISA检测大鼠海马组织TNF-α、IL-10、IL-6水平;试剂盒检测海马组织MDA、SOD、GSH-Px和CAT水平;Nissl染色观察大鼠海马组织形态变化;TUNEL染色检测海马组织神经元凋亡;Western blot检测Cleaved-caspase-3、Bax、Bcl-2、PI3K、AKT蛋白表达。结果:与CK组相比,Model组大鼠海马组织有明显损伤,大鼠潜伏期、海马组织中TNF-α、IL-6水平、MDA含量和Cleaved-caspase-3、Bax蛋白表达水平、神经元凋亡率显著升高,大鼠目标象限滞留时间和穿越平台次数、海马组织中IL-10水平、SOD、GSH-Px、CAT活性、Bcl-2、p-PI3K/PI3K、p-AKT/AKT蛋白表达水平显著降低(P<0.05);与Model组相比,ARC-L组和ARC-H组大鼠海马组织损伤明显减轻,大鼠潜伏期、海马组织中TNF-α、IL-6水平、MDA含量和Cleaved-caspase-3、Bax蛋白表达水平、神经元凋亡率显著降低,大鼠滞留时间和穿越平台次数、海马组织中IL-10水平、SOD、GSH-Px、CAT活性、Bcl-2、p-PI3K/PI3K、p-AKT/AKT蛋白表达水平显著升高(P<0.05);LY294002可减弱ARC对PTSD大鼠认知能力的改善作用(P<0.05)。结论:ARC可通过激活PI3K/AKT通路减轻PTSD大鼠炎症反应与氧化应激损伤,抑制神经元凋亡,进而改善其认知功能。
Objective:To investigate the effect of Arctigenin(ARC)on cognitive ability in rats with posttraumatic stress disorder(PTSD)by regulating PI3K/AKT signaling pathway.Methods:Rats were randomly separated into control(CK)group,Model group,ARC low-dose(ARC-L)group,ARC high-dose(ARC-H)group,and ARC high-dose+LY294002(ARC-H+LY294002)group.Morris water maze was applied to test spatial learning and memory abilities of rats;ELISA was applied to detect levels of TNF-α,IL-10 and IL-6 in hippocampal tissue;reagent kit was applied to detect levels of MDA,SOD,GSH-Px and CAT in hippocampal tissue;Nissl staining was performed to observe morphological changes in rat hippocampal tissue;TUNEL staining was applied to detect neuronal apoptosis in hippocampal tissue;Western blot was applied to detect expressions of Cleaved-caspase-3,Bax,Bcl-2,PI3K and AKT proteins.Results:Compared with CK group,hippocampal tissue of rats in Model group showed obvious damage,the latency period,levels of TNF-αand IL-6,MDA content,expression levels of Cleaved-caspase-3 and Bax proteins,and neuronal apoptosis rate in hippocampus of rats were obviously increased,while the residence time in the target quadrant and crossing platform frequency of rats,IL-10 level,SOD,GSH-Px,CAT activity,Bcl-2,p-PI3K/PI3K and p-AKT/AKT protein expression levels in hippocampal tissue were obviously reduced(P<0.05);compared with Model group,damage of hippocampal tissue in ARC-L and ARC-H groups of rats was obviously reduced,the latency period,levels of TNF-αand IL-6,MDA content,expression levels of Cleaved-caspase-3 and Bax proteins,and neuronal apoptosis rate in hippocampus of rats were obviously reduced,while residence time and crossing platform frequency of rats,IL-10 level,SOD,GSH-Px,CAT activity,Bcl-2,p-PI3K/PI3K and p-AKT/AKT protein expressions in hippocampal tissue were obviously increased(P<0.05);LY294002 was able to alleviate the improvement effect of ARC on cognitive ability in PTSD rats(P<0.05).Conclusion:ARC can alleviate the inflammatory response and oxidative stress damage in PTSD rats by activating PI3K/AKT pathway,inhibit neuronal apoptosis,and thereby improve their cognitive function.
作者
郑春光
郭文静
ZHENG Chunguang;GUO Wenjing(Department of Basic Medicine,Henan Vocational College of Nursing,Anyang 455000,China;School of Basic Medicine,Wenzhou Medical University,Wenzhou 325035,China)
出处
《中国免疫学杂志》
北大核心
2026年第2期316-321,共6页
Chinese Journal of Immunology
