刺槐素激活PPARγ/NF-κB通路改善高糖/高脂应激所致血管内皮细胞功能失调的研究  

Effect of Acacetin Activation of PPARγ/NF-κB Pathway on Vascular Endothelial Cell Dysfunction Induced by High Glucose/High Fat Stress

作　　者：甘璐 孙晓春[2] 彭国平 张洁[2] 熊绍风 饶毅[1] GAN Lu;SUN Xiaochun;PENG Guoping;ZHANG Jie;XIONG Shaofeng;RAO Yi(Jiangxi University of Chinese Medicine,Nanchang Jiangxi 330004,China;The First Affiliated Hospital of Nanchang University,Nanchang Jiangxi 330006,China;Jiangxi Institute of Applied Science and Technology,Nanchang Jiangxi 330100,China)

机构地区：[1]江西中医药大学,江西南昌330004 [2]南昌大学第一附属医院,江西南昌330006 [3]江西应用科技学院,江西南昌330100

出　　处：《药品评价》2023年第3期294-298,共5页Drug Evaluation

基　　金：江西省中医药管理局科技计划重点项目(2020Z016)。

摘　　要：目的研究刺槐素(ACA)对高糖/高脂(HG/HF,44/1.0 mmol/L)应激所致的血管内皮功能失调的保护作用及其机制。方法采用HG/HF应激诱导血管内皮细胞功能失调模型,采用细胞计数试剂盒8(CCK8)法、细胞划伤损伤实验、流式细胞术、分光光度法,从修复愈合、细胞凋亡、ET-1和NO水平等方面,探究ACA对HG/HF应激下的血管内皮细胞功能失调的保护与修复作用,并通过过氧化物酶体增殖物激活受体γ/核因子κB(PPARγ/NF-κB)信号通路抑制剂(T0070907)干预,考察ACA对HG/HF应激诱导血管内皮功能失调的保护与修复作用与PPARγ/NF-κB通路的关系。结果ACA在小于等于40μmol/L细胞存活率大于80%。HG/HF造成HUVECs细胞失调后,加入ACA(40μmol/L),人体脐静脉内皮细胞(HUVECs)细胞修复愈合能力显著提高,HUVECs细胞凋亡明显减少,ET-1含量减少,NO含量增加,证实ACA具有改善HG/HF应激诱导HUVECs细胞功能失调的作用。qRT-PCR结果显示PPARγ/NF-κB信号通路的mRNA表达上调,通过T0070907干预,ACA的改善作用也被逆转,进一步证实ACA是通过激活PPARγ/NF-κB发挥改善HG/HF应激造成的血管内皮细胞功能失调的作用。结论ACA通过激活PPARγ/NF-κB通路达到改善HG/HF应激诱导下的HUVECs功能失调的目的。Objective To investigate the protective effect of acacetin(ACA)on vascular endothelial dysfunction caused by HG/HF(44/1.0 mmol/L)stress and its related mechanism.Methods The endothelial cell dysfunction model was established by HG/HF stress.CCK8 method,cell scratch injury test,flow cytometry and spectrophotometry were used,the protective and repairing effects of ACA on endothelial cell dysfunction under HG/HF stress were explored from the aspects of healing and repair,apoptosis,ET-1 and NO levels,etc.By PPARγ/NF-κB pathway inhibitors(T0070907)intervention to investigate the relationship between the protective and repair effects of ACA on HG/HF stress-induced vascular endothelial dysfunction and the PPARγ/NF-κB pathway.Results ACA had a survival rate of more than 80%in cells less than or equal to 40μmol/L.When HG/HF stressed HUVECs were added with ACA(40μmol/L),the healing and repair displacement of cells was significantly improved;cell apoptosis decreased significantly;the content of ET-1 decreased and the content of NO increased.These results confirmed that ACA has the effect of improving the dysfunction of HUVECs cells induced by HG/HF stress.The mRNA expression of PPARγ/NF-κB signaling pathway was up-regulated by qRT-PCR.The improvement effect of ACA was also reversed by the T0070907 intervention,which further confirm that ACA can improve the function of endothelial cells induced by HG/HF stress by activating PPARγ/NF-κB.Conclusion ACA can improve the function of HUVECs under HG/HF stress by activating PPARγ/NF-κB pathway.

关 键 词：刺槐素 过氧化物酶体增殖物激活受体 NF-ΚB 内皮功能失常 血管内皮细胞 

分 类 号：R285[医药卫生—中药学]