Isorhamnetin attenuates TNF-α-induced inflammation, proliferation, and migration in human bronchial epithelial cells via MAPK and NF-κB pathways.

Isorhamnetin has distinct anti-inflammatory activity and inhibits cell proliferation and migration. These effects are also involved in the pathogenesis of asthma. However, the effect of isorhamnetin on bronchial epithelial cells in patients with asthma has not been examined. Cells of human bronchial epithelial cell line BEAS-2B were cultured with isorhamnetin and tumor necrosis factor (TNF)-α. The effects of isorhamnetin on BEAS-2B cell viability were assessed using CCK8 assay. The EdU (5-ethynyl-2'-deoxyuridine) cell proliferation assay was performed to assess cell proliferation. BEAS-2B cell migration was measured using Transwell and wound healing assays. Real-time PCR and enzyme-linked immunosorbent assay were conducted to measure the expression of pro-inflammatory cytokines. Protein expression levels were determined by western blotting. Immunofluorescence was used to detect nuclear translocation of nuclear factor kappa B (NF-κB). We found that isorhamnetin at 20 and 40 μM reduced the proliferation of BEAS-2B cells induced by TNF-α. Isorhamnetin significantly decreased the expression of interleukin (IL)-1β, IL-6, IL-8, and C-X-C motif chemokine ligand 10 in BEAS-2B cells induced by TNF-α. Additionally, 10 μM isorhamnetin effectively reduced cell migration induced by TNF-α. Treatment with isorhamnetin inhibited the phosphorylation of mitogen-activated protein kinase (MAPK) and NF-κB pathways induced by TNF-α. In summary, isorhamnetin inhibited the inflammation, proliferation, and migration of BEAS-2B cells by regulating the MAPK and NF-κB signaling pathways and is a drug candidate for asthma.