[Animal modeling] - Effect of quercetin on pulmonary fibrosis in rats and its related mechanism

  Objective To investigate the effects of quercetin on interstitial transformation, inflammation and NOX4-P62 signal pathway in lung tissue of rats with pulmonary fibrosis, and to provide experimental basis for further elucidating the mechanism of quercetin on pulmonary fibrosis.

  Methods The experimental rats were divided into control group, bleomycin group (BLM group) and bleomycin+quercetin group (BLM+QUE group). The appearance of lung tissue in each group was observed on the 7th, 14th and 28th days after modeling, and the pulmonary fibrosis was evaluated by hematoxylin eosin staining (HE staining). The reduced nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4), autophagic protein P62 and nuclear factor in lung tissue of each group were detected by Western blot κ B(NF- κ B) Protein expression of, reverse transcription polymerase chain reaction (qRT PCR) detection of vascular smooth muscle actin in human lung adenocarcinoma cell line A549( α- MRNA expression level of SMA) and E-cadherin, and detection of transforming growth factor by enzyme-linked immunosorbent assay (ELISA)- β 1(TGF- β 1) Interleukin-1 β (IL-1 β) And tumor necrosis factor- α (TNF- α) Level of. Results The pulmonary fibrosis of rats in BLM group was gradually aggravated with the increase of time. The symptoms of BLM+QUE group were lighter than those of BLM group on the 7th day, and were significantly relieved on the 28th day. TGF of BLM group- β 1、IL-1 β、 TNF- α、 NOX4、P62、NF- κ The expression of B protein was significantly higher than that of the control group (P<0. 7="" que="" blm="" p="">0. 05), but it was significantly lower than that of the BLM group at the 14th and 28th days (P<0. 05). Compared with the control group, TGF was added- β 1 of A549 cells E-cadherin α- The expression of SMA mRNA decreased and increased significantly (P<0.05); After administration of quercetin, E-cadherin α- SMA mRNA expression is higher than TGF- β In group 1, it was significantly increased and decreased (P<0.05).

  Conclusion Quercetin can inhibit TGF- β 1. It can change the interstitial transformation induced by human lung adenocarcinoma cell line A549, reduce the inflammatory reaction of rats with pulmonary fibrosis, and alleviate the pulmonary fibrosis induced by bleomycin. Autophagy activity is inhibited in the process of bleomycin induced pulmonary fibrosis in rats; Quercetin may inhibit the NOX4-P62 signal pathway, activate autophagy, and reduce pulmonary fibrosis in rats.