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
发布时间：2018-08-06 17:34
【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 000μg/mL)PM2.5处理正常人支气管上皮细胞(human bronchial epithelium cell line,HBE细胞)24h,台盼蓝拒染法测定细胞活力,采用200、400、600μg/mL PM2.5进行后续实验;设PM2.5(600μg/mL)单处理组、PARP-1抑制剂4-氨基-1,8-萘二胺(4-AN)(10μg/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、600μg/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、600μg/mL PM2.5处理组与DMSO对照组比较,差异有统计学意义(P0.05);4-AN预处理可拮抗PM2.5诱导的PARP-1表达与p65核转位升高,同时炎症介质NO与催化合成NO的iNOS水平显著下降(与PM2.5单处理组比较,差异有统计学意义,P0.05),并恢复至正常水平(与4-AN单处理组和对照组比较差异无统计学意义,P0.05)。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。
[Abstract]:Objective to investigate whether inhibiting poly ADP-ribose polymerase-1 (PARP-1) can alleviate / reverse the inflammatory response induced by fine particles (PM2.5). Methods the normal human bronchial epithelial cells (human bronchial epithelium cell lineage cells were treated with different concentration (0 000 渭 g/mL) PM2.5 for 24 h. The viability of the cells was determined by trypan blue exclusion method. 200400600 渭 g/mL PM2.5 was used for the follow-up experiment. The expression of p65 subunit of nuclear factor- 魏 B (NF- 魏 B), p65 subunit of nuclear factor- 魏 B (NF- 魏 B) and inducible nitric oxide synthase (iNOS) were detected by PM2.5 (600 渭 g/mL) single treatment group, 4-an PM2.5 group (10 渭 g/mL) single treatment group and solvent (DMSO) control group. Nitric oxide (no) levels were measured by nitrate reduction method. Results when HBE cells were treated with PM2.5 200400600 渭 g/mL alone, the survival rate of HBE cells decreased with the increase of PM2.5 concentration. The difference was statistically significant (P0.05) that pretreatment with 4-an could antagonize the increase of PARP-1 expression and p65 nuclear translocation induced by PM2.5, while the level of no and the iNOS of catalytic synthesis of no were significantly decreased (compared with PM2.5 single treatment group). The difference was statistically significant (P0.05), and returned to the normal level (compared with 4-AN single treatment group and control group, there was no significant difference (P0.05). Conclusion inhibition of PARP-1 can significantly alleviate the inflammatory effect of PM2.5 on HBE cells, and its mechanism is related to down-regulation of nuclear translocation of NF- 魏 B and blocking the expression of inflammatory mediators.
【作者单位】： 四川大学华西公共卫生学院环境卫生与职业医学系;
【基金】：国家自然科学基金(No.81372945)资助
【分类号】：R56
本文编号：2168474
[Abstract]:Objective to investigate whether inhibiting poly ADP-ribose polymerase-1 (PARP-1) can alleviate / reverse the inflammatory response induced by fine particles (PM2.5). Methods the normal human bronchial epithelial cells (human bronchial epithelium cell lineage cells were treated with different concentration (0 000 渭 g/mL) PM2.5 for 24 h. The viability of the cells was determined by trypan blue exclusion method. 200400600 渭 g/mL PM2.5 was used for the follow-up experiment. The expression of p65 subunit of nuclear factor- 魏 B (NF- 魏 B), p65 subunit of nuclear factor- 魏 B (NF- 魏 B) and inducible nitric oxide synthase (iNOS) were detected by PM2.5 (600 渭 g/mL) single treatment group, 4-an PM2.5 group (10 渭 g/mL) single treatment group and solvent (DMSO) control group. Nitric oxide (no) levels were measured by nitrate reduction method. Results when HBE cells were treated with PM2.5 200400600 渭 g/mL alone, the survival rate of HBE cells decreased with the increase of PM2.5 concentration. The difference was statistically significant (P0.05) that pretreatment with 4-an could antagonize the increase of PARP-1 expression and p65 nuclear translocation induced by PM2.5, while the level of no and the iNOS of catalytic synthesis of no were significantly decreased (compared with PM2.5 single treatment group). The difference was statistically significant (P0.05), and returned to the normal level (compared with 4-AN single treatment group and control group, there was no significant difference (P0.05). Conclusion inhibition of PARP-1 can significantly alleviate the inflammatory effect of PM2.5 on HBE cells, and its mechanism is related to down-regulation of nuclear translocation of NF- 魏 B and blocking the expression of inflammatory mediators.
【作者单位】： 四川大学华西公共卫生学院环境卫生与职业医学系;
【基金】：国家自然科学基金(No.81372945)资助
【分类号】：R56
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1 王静;PARP-1基因沉默对机械牵张诱导的人支气管上皮细胞炎性细胞因子表达的研究[D];山东大学;2014年
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