紫铆花素可通过调控微小RNA 485对缺氧诱导的大鼠神经细胞凋亡的影响  

Effects of butein on hypoxia-induced neuronal apoptosis in rats by regulating miR-485

作　　者：李梅芳[1] 杨晶[1] 王翠[1] 潘微[1] 金玉 卢菁 刘江华[1] 杨畅[1] 王琼[2] Li Meifang;Yang Jing;Wang Cui;Pan Wei;Jin Yu;Lu Jing;Liu Jianghua;Yang Chang;Wang Qiong(Department of Brain Diseases,Wuhan Traditional Chinese Medicine Hospital,Wuhan 430000,Hubei Province,China)

机构地区：[1]武汉市中医医院脑病科,430000 [2]武汉市中医医院内分泌科,430000

出　　处：《中华老年心脑血管病杂志》2023年第3期302-306,共5页Chinese Journal of Geriatric Heart,Brain and Vessel Diseases

基　　金：武汉市医学科研项目(WZ21C42,WZ21C58);武汉市卫生和计划生育委员会科研项目(WZ18D12)。

摘　　要：目的探讨紫铆花素对缺氧诱导的大鼠肾上腺嗜铬(PC12)细胞增殖、凋亡、炎性损伤的影响及其可能作用机制。方法建立缺氧诱导的PC12细胞损伤模型,随机分组:对照组、缺氧组、紫铆花素1组、紫铆花素2组、紫铆花素3组、阴性组、过表达组、紫铆花素3+对照组、紫铆花素3+抑制剂组(n=9);采用ELISA法检测白细胞介素(IL)-1β、IL-6、TNF-α水平;qRT-PCR法检测微小RNA 485(miR-485)表达量。结果与对照组比较,缺氧组细胞活性、miR-485表达明显降低,细胞凋亡率、IL-1β、IL-6、TNF-α水平明显升高(P<0.05);与缺氧组比较,紫铆花素1组、紫铆花素2组、紫铆花素3组细胞活性、miR-485表达明显升高,细胞凋亡率、IL-1β、IL-6、TNF-α水平明显降低(P<0.05);与阴性组比较,过表达组细胞活性明显升高,细胞凋亡率、IL-1β、IL-6、TNF-α水平明显降低(P<0.01);与紫铆花素3+对照组比较,紫铆花素3+抑制剂组细胞活性明显降低[(50.68±4.92)%vs(83.70±7.34)%,P<0.01],细胞凋亡率、IL-1β、IL-6、TNF-α水平明显升高[(15.74±1.19)%vs(10.56±1.06)%,(48.54±4.01)ng/L vs(30.20±2.35)ng/L,(72.44±6.37)ng/L vs(50.43±4.78)ng/L,(96.34±8.55)ng/L vs(71.29±6.82)ng/L,P<0.01]。结论紫铆花素可通过上调miR-485表达而促进PC12细胞存活并抑制细胞凋亡、炎性细胞因子表达从而减轻缺氧诱导的PC12细胞损伤。Objective To investigate the effect of butein on hypoxia-induced proliferation,apoptosis and inflammatory injury in a rat catecholamine-secreting pheochromocytoma cell line PC12 and its possible mechanism.Methods A hypoxia-induced injury model of PC12 cells was established and then randomly divided into Control group,Hypoxia group,Butein 1,2 and 3 groups(0.5,1,2μmol/L),negative group,overexpression group,Butein 3+control group,and Butein 3+inhibitor group(n=9).The levels of IL-1β,IL-6 and TNF-αwere detected by ELISA.The expression of miR-485 was detected by qRT-PCR.Results Compared with the Control group,the cell activity and expression of miR-485 were decreased,while the apoptotic rate and the levels of IL-1β,IL-6 and TNF-αwere increased in the Hypoxia group(P<0.05).Compared with Hypoxia group,the cell activity and miR-485 level were increased,while the apoptotic rate and IL-1β,IL-6 and TNF-αlevels were decreased in the 3 Butein groups(P<0.05).Compared with the negative group,the cell activity of the overexpression group was increased,while the apoptotic rate and the levels of IL-1β,IL-6 and TNF-αwere decreased in the overexpression group(P<0.01).Compared with the Butein 3+control group,the cell viability was decreased[(50.68±4.92)%vs(83.70±7.34)%,P<0.01],while the apoptotic rate and the levels of IL-1β,IL-6 and TNF-αwere increased in the Butein 3+inhibitor group[(15.74±1.19)%vs(10.56±1.06)%,48.54±4.01 ng/L vs 30.20±2.35 ng/L,72.44±6.37 ng/L vs 50.43±4.78 ng/L,96.34±8.55 ng/L vs 71.29±6.82 ng/L,P<0.01].Conclusion Butein could promote the survival of PC12 cells by up-regulating miR-485 and inhibit the apoptosis and expression of inflammatory cytokines,and thereby reduce hypoxia-induced PC12 cell damage.

关 键 词：微RNAS 低氧 炎症 细胞凋亡 

分 类 号：R285.5[医药卫生—中药学]