苦味素受体对PM_(2.5)染毒诱导支气管上皮细胞炎症反应的调节机制  

Regulatory mechanism of bitter taste receptor(T2Rs) in inflammatory response of airway epithelial cells induced by PM_(2.5)

作　　者：李琪[1] 周向东[1] 刘美花[1] 刘峰[1] 刘畅[1] LI Qi;ZHOU Xiang-dong;LIU Mei-hua;LIU Feng;LIU Chang(Department of Respiratory Medicine,the First Affiliaied Hospital,Hainan Medical University,Haikou,Hainan 570102,China)

机构地区：[1]海南医学院第一附属医院呼吸内科,海南海口570102

出　　处：《环境与健康杂志》2018年第9期765-767,F0003,共4页Journal of Environment and Health

基　　金：国家自然科学基金(81660010;81611530713);海南省卫生厅科研课题(16A200021);海南医学院培育基金(HY2016-16)

摘　　要：目的探讨苦味素受体(T2Rs)对PM_(2.5)染毒诱导气道炎症反应的调节机制。方法将支气管上皮细胞HBE16分为对照组、PM_(2.5)组(40μg/ml PM_(2.5))、PM_(2.5)+桔梗皂苷组(200 mg/L桔梗皂苷+40μg/ml PM_(2.5))、桔梗皂苷组(200 mg/L桔梗皂苷),经过处理或染毒后,分别采用细胞免疫荧光法、ELISA法和RT-PCR法检测各组支气管上皮细胞T2R14、白细胞介素4(IL-4)和肿瘤坏死因子-α(TNF-α)的表达水平。结果 PM_(2.5)组细胞IL-4、TNF-α的蛋白表达和mRNA水平明显高于对照组,差异有统计学意义(P<0.01);T2R14的蛋白表达和mRNA水平变化不明显。桔梗皂苷组细胞IL-4、TNF-α的蛋白表达和mRNA水平明显低于PM_(2.5)组,T2R14的蛋白表达和mRNA水平明显高于对照组,差异均有统计学意义(P<0.05或P<0.01)。结论中药的苦味成分可引起支气管上皮细胞T2R14激活,抑制慢性炎症气道的炎症因子产生和释放,提示T2R14可能参与苦味物质的抗炎过程。Objective To investigate the regulatory mechanism of bitter taste receptor(T2Rs) in the inflammatory response of airway epithelial cells induced by PM2.5 stimulation. Methods The bronchial epithelial cells were cultured with 40 μg/ml PM2.5 as the stimulator, or 200 mg/L platycodin as the intervention, the expression of T2R14, IL-4 and TNF-α in bronchial epithelial cells in each group was detected by cell immunofluorescence, ELISA and RT-PCR. Results The protein expression and mRNA levels of IL-4 and TNF-α in PM2.5 group were significantly higher than those in the control group(P<0.01), while the T2 R14 did not change significantly. The protein expression and mRNA levels of IL-4, TNF-α in the platycodin intervention group were evidently decreased compared with PM2.5 group(P<0.01), however, the T2R14 expression was significantly higher than that in the control group(P<0.05). Conclusion The components of bitter Chinese medicine can induce activating and expressing of T2R14 in bronchial epithelial cells and inhibit producing and releasing of inflammatory factors in chronic inflammatory airway,which demonstrates that T2R14 is involved in the anti-inflammatory process of bitter substances.

关 键 词：苦味素受体 PM2.5 炎症因子 气道炎症 

分 类 号：R994.6[医药卫生—毒理学]