摘要
Abstract
Objective To investigate the effect and mechanism of ursodeoxycholic acid on bronchial epithelial cell injury induced by toluene diisocyanate(TDI).Methods BEAS-2B cells were randomly divided into control group(conventional culture),TDI-human serum albumin(HSA)group(120.00 mg·L-1 TDI-HSA),low-dose group(100 μmol·L-1 ursodeoxycholic acid+120.00 mg·L-1 TDI-HSA),high-dose group(200 μmol·L-1 ursodeoxycholic acid+120.00 mg·L-1 TDI-HSA)and rapamycin group(25 nmol·L-1 rapamycin+120.00 mg·L-1 TDI-HSA).The expression of inflammatory factors was detected by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR)and enzyme-linked immunosorbent assay(ELISA);the level of reactive oxygen species(ROS)was detected by DCFH-DA;and the protein expression of each cell was detected by Western blot.Results The mRNA levels of interleukin(IL)-6 in control group,TDI-HSA group,low-dose group and high-dose group were 1.00±0.13,2.20±0.24,1.87±0.12,1.48±0.14,respectively;IL-8 levels were(22.65±1.96),(81.42±6.35),(56.36±5.88),(38.28±3.25)pg·mL-1,respectively;ROS levels were(100.00±3.47)％,(351.25±22.52)％,(312.80±26.59)％,(242.15±13.60)％,respectively;the protein levels of dynamic associated protein 1(DRP1)were 0.23±0.03,0.82±0.08,0.69±0.10,0.55±0.05,respectively;benzyl chloride 1(Beclin1)protein expression levels were 0.23±0.04,0.60±0.07,0.44±0.04,0.37±0.03,respectively;phosphorylated adenylate activates protein kinase(p-AMPK)protein expression levels were 0.20±0.05,0.49±0.05,0.40±0.03,0.34±0.04,respectively.Beclin1 protein expression levels in high-dose group and rapamycin group were 0.35±0.04 and 0.69±0.07,respectively;IL-6 levels were(17.63±1.36)and(29.52±3.49)pg·mL-1,respectively;IL-18 levels were(65.22±5.30)and(95.58±6.80)pg·mL-1,respectively.The above indexes:TDI-HSA group was compared with control group,low-dose group and high-dose group were compared with TDI-HSA group,rapamycin group compared with high dose group,the differences were significant(all P＜0.05).Conclusion Ursodeoxycholic acid may mediate ROS/AMPK/autophagy pathway to improve the inflammatory response and mitochondrial dysfunction induced by TDI-HSA.关键词
熊去氧胆酸/哮喘/甲苯二异氰酸酯/支气管上皮细胞/炎症反应/自噬Key words
ursodeoxycholic acid/asthma/toluene diisocyanate/bronchial epithelial cells/inflammatory response/autophagy分类
药学
