Amygdalin attenuates PM2.5-induced human umbilical vein endothelial cell injury via the TLR4/NF-κB and Bcl-2/Bax signaling pathways  

作　　者：Bixu Wang Tong Sun Ling Sun Lan Li Haitong Wan Zhishan Ding Xiaoqing Ye 

机构地区：[1]School of Medical Technology and Information Engineering,Zhejiang Chinese Medical University,Hangzhou 310053,China [2]School of Life Sciences,Zhejiang Chinese Medical University,Hangzhou 310053,China

出　　处：《Acta Biochimica et Biophysica Sinica》2022年第10期1476-1485,共10页生物化学与生物物理学报（英文版）

基　　金：supported by the grants from the National Key Research and Development Program of China(No.2019YFC1708604);Zhejiang Provincial Natural Science of Foundation of China(No.LQ20B070005);the National Natural Science Foundation of China(No.22106143);Zhejiang Provincial Fund for Outstanding Young Talents of Traditional Chinese Medicine(No.2020ZQ013).

摘　　要：Mounting evidence supports that long-term exposure to fine particle pollutants(PM2.5)is closely implicated in cardiovascular diseases,especially atherosclerosis.Amygdalin is reported to attenuate external stimuli-induced cardiovascular diseases.However,the underlying mechanisms are still not understood.In this study,we aim to explore the protective effects of amygdalin on PM2.5-induced human umbilical vein endothelial cell(HUVEC)injury and unravel the specific mechanisms by MTT,DCFH-DA,biochemical,immunofluorescence,ELISA,RT-qPCR,flow cytometry,TUNEL and western blot analysis.The results reveal that amygdalin reverses PM2.5-induced cytotoxicity and attenuates intracellular ROS production.Moreover,amygdalin increases the levels of SOD and GSH and alleviates the MDA content.Additionally,amygdalin causes a decline of IL-6,IL-1β,TNF-αand COX-2 levels.Moreover,amygdalin inhibits NF-κB p50 and TLR4 protein expressions and NF-κB p65 nuclear translocation.Concomitantly,a decline of phospho-NF-κB p65/NF-κB p65 and phospho-IκB-α/IκB-αis detected.Meanwhile,amygdalin pretreatment reduces HUVEC apoptosis.In addition,amygdalin triggers an upregulation of Bcl-2 and a downregulation of Bax after stimulation with PM2.5.Collectively,these results suggest that amygdalin suppresses PM2.5-induced HUVEC injury by regulating the TLR4/NF-κB and Bcl-2/Bax signaling pathways,indicating that amygdalin may be a novel target for atherosclerosis treatments.

关 键 词：AMYGDALIN PM2.5 INFLAMMATION oxidative stress APOPTOSIS 

分 类 号：R329.2[医药卫生—人体解剖和组织胚胎学]