期刊导航

论文摘要

PARP-1抑制对PM2.5致人支气管上皮细胞炎症反应的保护作用

The Protective Effect of Inhibition of PARP-1 on Inflammation Induced by PM2.5 in Human Bronchial

作者:黄庆, 张晶晶, 张遵真

Author:HUANG Qing, ZHANG Jing-jing, ZHANG Zun-zhen

收稿日期:          年卷(期)页码:2016,47(6):825-829

期刊名称:四川大学学报(医学版)

Journal Name:JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCE EDITION)

关键字:多聚二磷酸腺苷核糖多聚酶-1(PARP-1) PM2.5 炎症 NF-κB

Key words:Poly ADP-ribose polymerase-1 (PARP-1) PM2.5 Inflammation NF-κB

基金项目:

中文摘要

目的 研究抑制多聚二磷酸腺苷核糖多聚酶-1(poly ADP-ribose polymerase-1, PARP-1)是否能缓解/逆转细颗粒物(PM2.5)诱导的炎症反应。方法 以不同质量浓度(0~1 000 μg/mL)PM2.5处理正常人支气管上皮细胞(human bronchial epithelium cell line, HBE细胞)24 h,台盼蓝拒染法测定细胞活力,采用200、400、600 μg/mL PM2.5进行后续实验;设PM2.5(600 μg/mL)单处理组、PARP-1抑制剂4-氨基-1,8-萘二胺(4-AN)(10 μg/mL)单处理组、4-AN+PM2.5组、溶剂(DMSO)对照组,免疫印迹法检测PARP-1、核因子κ-B(NF-κB)的p65亚基和诱导型一氧化氮合酶(iNOS)表达水平,硝酸酶还原法检测一氧化氮(nitric oxide, NO)水平。结果 PM2.5 200、400、600 μg/mL单独处理HBE细胞时,细胞存活率随着PM2.5质量浓度增高而下降,PARP-1、p65核转位、iNOS和NO水平升高,400、600 μg/mL PM2.5处理组与DMSO对照组比较,差异有统计学意义(PPP>0.05)。 结论 抑制PARP-1可以明显缓解PM2.5对HBE细胞的致炎作用,其机制与下调NF-κB核转位进而阻断炎症介质表达有关。

英文摘要

Objective To explore whether the inhibition of poly ADP-ribose polymerase-1(PARP-1) could attenuated inflammation induced by fine particulate matter (PM2.5) in human bronchial epithelial cell line. Methods Cell viability was detected by Trypan Blue assay after incubated with PM2.5 for 24 h. PM2.5 doses no more than 600 μg/mL were utilized in the following experiments. In order to observe how PARP-1 would effect the expression of nuclear factor-κB p65 and inducible nitric oxide synthase (iNOS), cells were respectively treated with 600 μg/mL PM2.5, 10 μmol/L 4-amino-1,8-naphthalimide (4-AN), 600 μg/mL PM2.5+10 μmol/L 4-AN or DMSO. Western blot assay was used to estimate the protein expression of PARP-1, p65 in nuclear and iNOS in cytoplasm. Nitric acid enzyme reduction assay was used to determine the production of nitric oxide (NO). Results As the PM2.5 concentration increased, the cell viability decreased, while the expression of PARP-1, p65, iNOS and NO increased significantly (PP>0.05). Conclusion Inflammation triggered by PM2.5 could be attenuated by the inhibition of PAPR-1, which involved the block of transcriptional activity of NF-κB for inflammatory mediator.

关闭

Copyright © 2020四川大学期刊社 版权所有.

地址:成都市一环路南一段24号

邮编:610065