In the present study, the effects of albiflorin (ALB) on the pulmonary inflammation induced by ovalbumin (OVA) in an asthmatic mouse model were investigated. Airway hyperreactivity (AHR) in asthmatic mice was detected using the acetylcholine stimulation test. Eosinophilia cells in the serum of asthmatic mice were counted. Hematoxylin and eosin (H&E) staining was used to observe pathological changes in lung tissue. Inflammatory cytokines, including interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were detected in bronchoalveolar lavage fluid (BALF) and lung tissue using enzyme-linked immunosorbent assay (ELISA). Western blotting was used to detect the mitogen-activated protein kinase/nuclear factor kappa B (MAPK/NF-κB) signaling pathway in the lungs of asthmatic mice. The results from the present study indicated that ALB dramatically suppressed the expression of inflammatory cytokines including IL-1β, IL-6, and TNF-α, and inflammatory cells. In addition, ALB significantly decreased malondialdehyde (MDA) content as well as increased superoxide dismutase (SOD) activity. ALB also alleviated AHR in asthmatic mice and improved pathological changes in the lungs. In addition, ALB inhibited the MAPK/NF-κB signaling pathway in the lungs of the asthmatic mice. Thus, ALB appears to inhibit lung inflammation in asthmatic mice via regulation of the MAPK/NF-κB signaling pathway.
Keywords: Albiflorin; MAPK; NF-κB; asthma; inflammation.
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