Abstract

Purpose Emodin has a protective effect on asthma. Obesity is closely related to asthma. We further explored the role of Emodin in obese asthmatic rats. Methods Ovalbumin (OVA) was used to induce asthma model, and high fat diet (HFD) was used to induce obese rat model. Body weight was measured before and after the modeling. Serum lipid levels were evaluated using commercial kits. Then, lung tissue and airway tissue of rat were separated for in vivo . Hematoxylin-eosin staining (HE) analyzed the extent of lung lesions. Quantitative reverse transcription PCR assessed the mRNA expression of Visfatin and Enzyme linked immunosorbent assay measured NF-κB protein expression in airway tissues. MTT, Brdu and Western blot detected cell viability, proliferation and NF-κB level of human bronchial epithelial cells 16HBE, respectively. Results Asthma and Emodin alone had no effect on the body weight of normal rats, while HFD promoted the body weight of rats and could be reversed by Emodin. Both asthma and obesity promoted the pathological damage of rat lungs, including emphysema, lipid accumulation, edema changes, lymphoid hypertrophy and airway smooth muscle hyperplasia as well as lipid accumulation in surum, and Emodin treatment could reduce the damage. In the airway tissues of asthma and obesity models, up-regulated Visfatin mRNA and NF-κB protein were observed. In 16HBE, Emodin reversed Visfatin’s role in promoting cell viability, proliferation and activating NF-κB signaling pathway. Conclusion Emodin inhibited NF-κB expression to relieve the pathological symptoms of obese asthmatic rats by Visfatin.