桑麻宣肺止咳方对感染后咳嗽大鼠气道炎症和氧化应激的影响OA

Objective To investigate the ameliorative effect and the related mechanism of Xuanfei Zhike Formula(SMXFZKF)on airway inflammation in rats with post-infectious cough(PIC).Methods Sixty male SD rats were randomly divided into a normal group,a model group,a low-,medium-,and high-dose SMXFZ-KF groups,and a positive control group.Except for the normal group,PIC rat models were established in the other groups using smoke inhalation+intranasal lipopolysaccharide(LPS)+capsaicin aerosol exposure.Coug-hing behavior was observed.Pathological changes in lung tissues were examined by using hematoxylin-eosin(HE)staining.Serum levels of interleukin-1β(IL-1β),interleukin-6(IL-6),and tumor necrosis factor-α(TNF-α)were measured by using enzyme-linked immunosorbent assay(ELISA).Serum concentrations of ma-londialdehyde(MDA),superoxide dismutase(SOD),and catalase(CAT)were determined by using assay kits.Protein expression of nuclear factor-κB(NF-κB),caspase-1,IL-1β,and interleukin-18(IL-18)in lung tissue was detected by Western blot.Results Compared with the normal group,the model group showed significant inflammatory cell infiltration in lung tissues and airways,significantly elevated serum levels of the in-flammatory cytokines IL-1β,IL-6,and TNF-α(P<0.05),marked elevated MDA content in lung tissue,and notable reduced levels of CAT and SOD(P<0.05).The expression of inflammation-related proteins NF-κB,caspase-1,IL-1β,and IL-18 in lung tissue was significantly increased(P<0.05).Compared with the model group,SMXFZKF alleviated pathological changes such as airway inflammation in the lung tissues of PIC model rats,reduced serum levels of IL-1β,IL-6,TNF-α,and MDA,increased the contents of CAT and SOD,and down-regulated the expression of NF-κB,caspase-1,IL-1β,and IL-18 in lung tissues.Conclu-sion Xuanfei Zhike Formula may effectively alleviate coughing symptoms in PIC rats by down-regulating the expression of NF-κB,caspase-1,IL-1β,and IL-18,thereby inhibiting the secretion of inflammatory factors and alleviating pathological changes in lung tissues.