Jiahao Li, He Li, Qian Zhang, Junnan Yue, Fan Zhang, Fangling Wang, Bin Tang, Hongxia Ma
This bioactive peptide protects against airway inflammation in OVA-induced asthmatic mice, an effect associated with the concurrent inhibition of NF-κB and p38 MAPK phosphorylation. Given the known cross-talk between these signaling pathways, the suppression of NF-κB may be partially mediated through the inhibition of p38 MAPK, although the precise underlying mechanism warrants further investigation. These findings provide experimental evidence supporting the potential application of this peptide as a novel therapeutic agent for bronchial asthma.
BACKGROUND: Bronchial asthma is a chronic heterogeneous respiratory disease characterized by persistent airway inflammation, airway hyperresponsiveness and mucus hypersecretion. Bioactive peptides are hydrolytic fragments of proteins or artificially synthesized products, and their effects on bronchial asthma have not been reported previously. In this study, a mouse model of asthma was established via ovalbumin (OVA) stimulation.
METHODS: Bronchoalveolar lavage fluid (BALF) was collected from OVA-challenged mice and subjected to cell counting. The levels of Th2 cytokines and pro-inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA). Hematoxylin and eosin (HE) staining was adopted to observe pathological alterations in lung tissue. Western blot analysis was performed to detect the protein expression levels of NF-κB, phosphorylated NF-κB, p38 MAPK and phosphorylated p38 MAPK in lung tissue.
RESULT: We found that bioactive peptides exerted beneficial therapeutic effects on asthma. Intervention with bioactive peptides, in a dose-dependent manner, attenuated airway hyperresponsiveness, reduced the count of inflammatory cells in BALF, downregulated the levels of pro-inflammatory cytokines, mitigated pathological damage to lung tissue, and markedly suppressed the phosphorylation of NF-κB and p38 MAPK without altering their total protein expression. Notably, the efficacy of the high-dose Spleen Aminopeptide group was comparable to that of dexamethasone.
CONCLUSION: This bioactive peptide protects against airway inflammation in OVA-induced asthmatic mice, an effect associated with the concurrent inhibition of NF-κB and p38 MAPK phosphorylation. Given the known cross-talk between these signaling pathways, the suppression of NF-κB may be partially mediated through the inhibition of p38 MAPK, although the precise underlying mechanism warrants further investigation. These findings provide experimental evidence supporting the potential application of this peptide as a novel therapeutic agent for bronchial asthma.