青岛大学学报（医学版）2025，Vol.61Issue(6)：800-806,7.DOI:10.11712/jms.2096-5532.2025.61.192
PRKCB对Aβ1-42诱导SH-SY5Y细胞损伤的保护作用
Protective effect of protein kinase Cβ against SH-SY5Y cell damage induced by amyloid β1-42
摘要
Abstract
Objective To investigate the protective effect and mechanism of protein kinase Cβ(PRKCB)against SH-SY5Y cell damage induced by amyloid β1-42(Aβ1-42).Methods SH-SY5Y cells were treated with Aβ1-42 to establish an in vitro model of Alzheimer's disease(AD),and then the experimental cells were randomly divided into Control group,Aβ1-42group,Aβ1-42+Vector group,and Aβ1-42+oe-PRKCB group.RT-qPCR and Western blot were used to measure the mRNA and protein expression levels of PRKCB;MTT assay,flow cytometry,and TUNEL staining were used to measure cell viability and apoptosis;related kits were used to measure the level of reactive oxygen species(ROS),the content of malondialdehyde(MDA),and the activity of su-peroxide dismutase(SOD);ELISA was used to measure the levels of interleukin-6(IL-6),interleukin-1β(IL-1β),and tumor nec-rosis factor-α(TNF-α);Western blot was used to measure the levels of extracellular signal-regulated kinase(ERK),c-Jun N-ter-minal kinase(JNK),and P38 mitogen-activated protein kinase(P38)in the mitogen-activated protein kinase(MAPK)pathway,as well as the levels of their phosphorylated proteins.Results Compared with the Control group,the Aβ1-42 group had signifi-cant reductions in the mRNA and protein expression levels of PRKCB(t=6.75,13.94,P＜0.001).Overexpression of PRKCB ef-fectively reversed the downregulation of PRKCB induced by Aβ1-42,increased cell viability,and reduced cell apoptosis rate and the number of TUNEL-positive cells(F=15.97-762.10,P＜0.05).PRKCB overexpression also enhanced the activity of SOD and re-duced the levels of ROS,MDA,IL-1β,IL-6,and TNF-α(F=18.41-279.30,P＜0.05).In addition,PRKCB overexpression spe-cifically downregulated the protein expression levels of p-ERK,ERK,p-JNK,and JNK in the ERK/JNK signaling pathway(F=22.30-44.61,P＜0.001),but with no significant effect on P38 protein.Conclusion PRKCB overexpression exerts a neuro-protective effect by inhibiting the ERK/JNK signaling pathway and alleviating oxidative stress,inflammatory response,and apoptosis in SH-SY5Y cells induced by Aβ1-42.关键词
阿尔茨海默病/蛋白激酶Cβ/淀粉样β肽类/MAP激酶信号系统/细胞凋亡/炎症Key words
Alzheimer disease/protein kinase C beta/amy-loid beta-peptides/MAP kinase signaling system/apoptosis/inflam-mation分类
医药卫生引用本文复制引用
张泽靖,马莉,邓燕,陆志星,李慧..PRKCB对Aβ1-42诱导SH-SY5Y细胞损伤的保护作用[J].青岛大学学报（医学版）,2025,61(6):800-806,7.基金项目
云南省教育厅青年人才基础研究项目(2024-J0313) （2024-J0313）
云南省科技人才与平台计划(院士专家工作站)(2023-05AF150024) （院士专家工作站）
云南省重点研发计划(202303AC100027) （202303AC100027）
云南省创新引导与科技型企业培育计划(202304BQ040019) （202304BQ040019）
