Protective effect of emodin on rats with pulmonary fibrosis and its partial mechanisms / 中国药理学通报

ABSTRACT

Aim To observe the influence of emodin on bleomycin-induced pulmonary fibrosis in rats, and explore its protective mechanisms. Methods Sixty SD rats were randomly divided into normal control group, sham operation group, model group, low-dose inter-vention group, high-dose intervention group and pred-nisone group. Each group included 10 animals. Rats in the latter 4 groups were intratracheally administered with bleomycin to establish pulmonary fibrosis model. From the second day, rats in low-and high-dose inter-vention groups were intragastrically treated with 2 mL of 20 and 80 mg · kg-1 emodin, respectively. Predni-sone group were intragastrically administrated with 2 mL of 5 mg·kg-1 prednisone acetate. However, con-trol and model groups were treated with 2 mL of normal saline. All rats were sacrificed on day 28. Pulmonary tissues were then removed, and HE and Masson stai-ning were performed. The contents of hydroxyproline ( HYP ) , malondialdehyde ( MDA ) , superoxide dis-mutase ( SOD) , glutathione-peroxidase ( GSH-Px) and catalase (CAT) in pulmonary tissues were measured. Serum concentrations of tumor necrosis factor-α ( TNF-α) , interleukin ( IL )-6 and IL-17 were detected by enzyme linked immunosorbent assay ( ELISA ) . The expression of Kelch-like ECH-associated protein 1 ( Keap 1 ) , nuclear factor-erythroid 2-related factor 2 (Nrf2) and nuclear factor-κB (NF-κB) p65 in pulmo-nary tissues was analyzed using Western blot. Results The pulmonary inflammation and fibrosis in low-and high-dose intervention as well as prednisone groups was significantly improved when compared with model group ( P0. 05 ) . Conclusion Emodin may protect against rats with pulmonary fibrosis by enhan-cing antioxidative ability and inhibiting inflammatory response.