Effects of epigallocatechin-3-gallate on the HMGB1/RAGE pathway in PM_2.5-exposed asthmatic rats.

Current studies have shown that long-term exposure to fine particulate matter (PM_2.5) can aggravate lung injury in asthmatic children. The pathway may play an important role, but few studies on the HMGB1/duanyu1648 signaling pathway in PM_2.5-induced asthma have been performed. Epigallocatechin-3-gallate (EGCG), which has antioxidant, anti-inflammatory and immunomodulatory effects, has not been examined in studies at home and abroad. In this study, we established an animal model of asthma and observed that the lung tissue was damaged, inflammatory cells infiltrated, bronchial wall thickness (WTt) and bronchial smooth muscle thickness (WTm) increased and the HMGB1 and mRNA and protein expression increased. The asthmatic rats exposed to PM_2.5 showed significantly increased lung injury and inflammatory cell infiltration, WTt and WTm further increased, and HMGB1 and duanyu1648 mRNA and protein levels were higher than those in the asthma group. The asthmatic rats exposed to PM_2.5 were treated with EGCG, which alleviated the lung injury, reduced the number of inflammatory cells, decreased WTt and WTm, and reduced the expression of HMGB1 and duanyu1648 mRNA and protein. The high-dose group showed more significant effects than the other groups. In conclusion, our results suggest that HMGB1 and duanyu1648 are involved in the pathogenesis of asthma. PM_2.5 exposure significantly aggravated airway inflammation injury in asthmatic rats. EGCG can reduce lung injury and airway remodeling in PM_2.5-exposed asthmatic rats and has lung protective effects. The mechanism may be related to regulation of the HMGB1/duanyu1648 signaling pathway. Our results may provide new ideas and methods for the prevention and treatment of PM_2.5-induced asthma.

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