PARP-1抑制對PM2.5致人支氣管上皮細胞炎癥反應(yīng)的保護作用
發(fā)布時間：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)是否能緩解/逆轉(zhuǎn)細顆粒物(PM2.5)誘導的炎癥反應(yīng)。方法以不同質(zhì)量濃度(0~1 000μg/mL)PM2.5處理正常人支氣管上皮細胞(human bronchial epithelium cell line,HBE細胞)24h,臺盼藍拒染法測定細胞活力,采用200、400、600μg/mL PM2.5進行后續(xù)實驗;設(shè)PM2.5(600μg/mL)單處理組、PARP-1抑制劑4-氨基-1,8-萘二胺(4-AN)(10μg/mL)單處理組、4-AN+PM2.5組、溶劑(DMSO)對照組,免疫印跡法檢測PARP-1、核因子κ-B(NF-κB)的p65亞基和誘導型一氧化氮合酶(iNOS)表達水平,硝酸酶還原法檢測一氧化氮(nitric oxide,NO)水平。結(jié)果 PM2.5 200、400、600μg/mL單獨處理HBE細胞時,細胞存活率隨著PM2.5質(zhì)量濃度增高而下降,PARP-1、p65核轉(zhuǎn)位、iNOS和NO水平升高,400、600μg/mL PM2.5處理組與DMSO對照組比較,差異有統(tǒng)計學意義(P0.05);4-AN預(yù)處理可拮抗PM2.5誘導的PARP-1表達與p65核轉(zhuǎn)位升高,同時炎癥介質(zhì)NO與催化合成NO的iNOS水平顯著下降(與PM2.5單處理組比較,差異有統(tǒng)計學意義,P0.05),并恢復(fù)至正常水平(與4-AN單處理組和對照組比較差異無統(tǒng)計學意義,P0.05)。結(jié)論抑制PARP-1可以明顯緩解PM2.5對HBE細胞的致炎作用,其機制與下調(diào)NF-κB核轉(zhuǎn)位進而阻斷炎癥介質(zhì)表達有關(guān)。
[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.
【作者單位】： 四川大學華西公共衛(wèi)生學院環(huán)境衛(wèi)生與職業(yè)醫(yī)學系;
【基金】：國家自然科學基金(No.81372945)資助
【分類號】：R56
本文編號：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.
【作者單位】： 四川大學華西公共衛(wèi)生學院環(huán)境衛(wèi)生與職業(yè)醫(yī)學系;
【基金】：國家自然科學基金(No.81372945)資助
【分類號】：R56
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1 王靜;PARP-1基因沉默對機械牽張誘導的人支氣管上皮細胞炎性細胞因子表達的研究[D];山東大學;2014年
，本文編號：2168474
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