枸杞多糖通过PI3K/Akt/mTOR通路调节自噬减轻β淀粉样蛋白1～40对HT22细胞的损伤  

Lycium barbarum Polysaccharide regulated autophagy through PI3K/Akt/mTOR pathway to attenuate the damage of Aβ1～40 injury to HT22 cells

作　　者：李海宁[1] 马婷婷[1] 王妍柏[1] 成江[1] LI Haining;Ma Tingting;WANG Yanbo;CHENG Jiang(The General Hospital of Ningxia Medical University,Yinchuan 750004,China)

机构地区：[1]宁夏医科大学总医院神经病学中心

出　　处：《宁夏医学杂志》2019年第10期872-875,864,共4页Ningxia Medical Journal

基　　金：宁夏自然科学基金项目(NZ17155)

摘　　要：目的探讨枸杞多糖(LBP)通过PI3K/Akt/mTOR通路调节自噬减轻β淀粉样蛋白1~40对HT22细胞的损伤的机制。方法将HT22细胞分为5组:对照组,模型组,高、中、低剂量LBP治疗组(40、20和10 mg/L)。模型组为Aβ1~4040μg/L处理细胞24 h;高、中、低剂量LBP治疗组为LBP处理HT22细胞24 h,加入β1~40 40μg/L继续孵育24 h。CCK8法用以检测细胞存活率,qRT-PCR检测自噬相关基因的表达,Western blot检测自噬相关蛋白及PI3K/Akt/mTOR通路蛋白的表达。结果与对照组相比,模型组细胞生存率降低,Beclin 1及LC3B mRNA及蛋白表达水平降低,p62、p-Akt及p-mTOR蛋白水平升高;与模型组相比,LBP高、中、低剂量组均可提高细胞存活率,LBP高剂量组可升高Beclin1及LC3B mRNA及蛋白水平,降低p62、p-Akt及p-mTOR蛋白水平。结论 LBP可逆转Aβ诱导HT22细胞的自噬抑制状态,其保护作用可能与抑制PI3K/Akt/mTOR信号通路激活有关。Objective To clarigy the effects of Lycium barbarum Polysaccharide(LBP) on autophay of HT22 cells injured by Aβ1~40 and investigate its possible mechanism.Methods HT22 cells were divided into 5 groups:control group,model group and LBP groups(10,20,40 mg/L). The model group was treated with Aβ1~4 040μg/mL for 24 h. LBP(10,20,40 mg/L) were given 24 h prior to Aβ1~4 040 μg/mL incubation and maintained for 24 h post-Aβ1~40 treatment. After treatments,CCK8 assay was used to detected the HT22 cell viability. qRT-PCR was used to detect the expression of autophagy-related genes,Western blot was used to detect the expression of autophagy-related proteins and PI3 K/Akt/mTOR pathway proteins.Results Compared with the control group,the survival rate of the model group was lower. The levels of Beclin1,LC3 B mRNA were decreased and the levels of Beclin1,LC3 B II protein were decreased,while p62,p-Akt and p-mTOR protein levels increased in model group compared with control group. Compared with the model group,the different groups of LBP could improve the cell survival rate,while the high dose group of LBP could increase the levels of Beclin1 and LC3 B mRNA and protein,and decrease the level of p62,Akt and p-mTOR protein. P-Akt and p-mTOR protein levels.Conclusion LBP can reverse the autophagy inhibition induced byAβ1~40 in HT22 cells,which may be related to the inhibition of PI3 K/Akt/mTOR signaling pathway activation.

关 键 词：枸杞多糖 Β淀粉样蛋白 阿尔茨海默病 自噬 PI3K/Akt/mTOR信号通路 

分 类 号：R742[医药卫生—神经病学与精神病学]