Glaucocalyxin A alleviates ovalbumin-induced airway inflammation through HMGB1/TLR4/NF-κB signaling pathway in asthmatic mice / 国际药学研究杂志

ABSTRACT

Objective: To investigate the therapeutic effect of glaucocalyxin A(GLA)on airway inflammation in a mouse mod- el of ovalbumin(OVA)-induced asthma and whether the mechanism is associated with the HMGB1/TLR4/NF-κB signaling pathway. Methods: Forty BALB/c mice were divided into 5 groups(8 mice in each group):control group, OVA model group, GLA-L group (10 mg/kg), GLA-H group(40 mg/kg)and dexamethasone group(1 mg/kg). HE and PAS staining were used to observe the inflammatory infiltration and the number of goblet cells in mouse lung tissue;Diff-Quick staining was used to count various cell types in mouse bronchoalveolar lavage fluid(BALF);ELISA was used to detect the content of inflammatory and pro-inflammatory cytokines in mouse BALF;Western blotting(WB)was used to detect the expression of HMGB1, TLR4, MyD88, NF-κB(nuclear)and NF-κB(cytosol)in lung tissue;immunohistochemistry was used to detect the expression level of HMGB1, TLR4 and NF-κB p65 protein in mouse lung tissue. Results: GLA reduced inflammatory cell exudation and goblet cell proliferation in OVA-induced asthmatic model;GLA treatment significantly decreased eosinophils, neutrophils and lymphocytes in BALF of asthmatic mice, and reduced the levels of pro-inflammatory cytokines(P<0.05);WB results showed that GLA inhibited the protein expression of HMGB1, TLR4, MyD88 and NF-κB(nuclear)(P<0.05);immunohistochemistry results showed that GLA reduced the expression of HMGB1, TLR4 and NF-κB p65 protein in lung tissue(P<0.05). Conclusion: GLA could ameliorate the OVA-induced airway inflammation in asthmatic mice, possibly via interfering in the HMGB1/TLR4/NF-κB signaling pathway.