Rhoifolin Improves Bleomycin-induced Fibrosis in Vivo and in Vitro through NRF2/HO-1 Pathway

Abstract

Abstract Purpose: An investigation shows that COVID-19's convalescing pulmonary lesions will experience varying degrees of fibrosis after being inspected by an imaging test. Traditional Chinese medicine frequently treats pulmonary fibrosis using honeysuckle. Rhoifolin (ROF), which is in large amounts of honeysuckle and has some anti-inflammatory qualities, has yet to be researched to see if it also has anti-fibrosis properties. This investigation will examine the main mechanism and see if rhoifolin can alleviate experimental lung fibrosis. Methods: Bleomycin was used to establish the lung fibrosis model in SD rats, and the effects of ROF on lung histopathology and appearance, as well as PCR measurements, were observed. Expression levels were determined by Western blot analysis. Bleomycin and LPS were used to cause pulmonary fibrosis and inflammation in A549 lung epithelial cells. Related mRNA were measured using real-time PCR following treatment with BLM and LPS, respectively. A western blot was performed to identify the signal pathway's activation. Results: The results showed that ROF lessened lung tissue damage in rats with pulmonary fibrosis. Reduce the level of pulmonary fibrosis in rat lung tissue and increase SMAD7 and HO-1 protein expression while lowering N-cadherin protein expression in vivo. In an in vitro experiment, A549 cells were modeled using BLM and LPS, respectively. ROF may decrease the relative protein expression of N-cadherin, P-JAK1, P-IKKβ, and PP65 while increasing Nrf2, Smad7, and HO-1 protein expression. Conclusion: The findings of this study provide proof that ROF has a strong inhibitory effect on pulmonary fibrosis and that its mechanism is closely linked to the NRF2/HO-1 pathway. As a result, our research provides robust experimental support for the potential use of ROF as a potential therapeutic agent for ameliorating pulmonary fibrosis.