To investigate the effect and mechanism of ursodeoxycholic acid on bronchial epithelial cell injury induced by toluene diisocyanate (TDI).

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.

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).

Ursodeoxycholic acid may mediate ROS/AMPK/ autophagy pathway to improve the inflammatory response and mitochondrial dysfunction induced by TDI-HSA.