Study on the mechanism of action of Pholidota chinensis polysaccharides on Pseudomonas aeruginosa induced pulmonary infection in rats
Objective To explore the inhibitory effect of Pholidota chinensis polysaccharides(PCP)on Pseudomonas aeruginosa(PA)induced pulmonary infection in a rat model and to preliminarily explore its possible mechanism of action.Methods A rat model of PA induced pulmonary infection was established:48 male SD rats were anesthetized by intraperitoneal injection of chloral hydrate,and tracheostomy was performed,and PA was injected into trachea.Rats were randomly divided into high-dose,medium,and low-dose PCP groups and model groups,with 12 rats in each group,another 12 untreated rats were used as blank control group.Rats in low,medium and high-dose PCP groups were given PCP 15 mg/kg,20 mg/kg and 30 mg/kg daily by gavage for 7 days,while rats in model group and blank control group were given normal saline by gavage at a weight of 5 ml/kg daily.On the day after the last medication,anesthetized rats were intraperitoneally injected with chloral hydrate.Lung tissue and alveolar lavage fluid were collected,and the wet dry weight ratio of lung tissue was measured.The total number of white blood cells in bronchoalveolar lavage fluid(BALF)of each group was counted.The supernatant of BALF was centrifuged to detect the expression levels of cytokines such as heparin binding protein,interleukin-6(IL-6),and procalcitonin(PCT).The phosphorylation expression levels of NF-κB and other proteins in BALF were detected using Western blotting(WB).Results Compared with the blank group,the wet dry weight ratio of lung tissue in the model group significantly increased(P<0.05),the number of white blood cells in alveolar lavage fluid significantly increased(P<0.05),and the expression of heparin binding protein,interleukin-6,procalcitonin and other proteins significantly increased(P<0.05),which can induce NF-κB p65 and p-1κB α phosphorylation in the lung tissue of the model group(P<0.05).PCP treatment of PA induced pulmonary infection in SD rat model can significantly inhibit NF-κB p65 and p-1κB α phosphorylation(P<0.05),and the indicators of action in the low,medium,and high-dose groups showed a gradient change(P<0.05).Conclusion The protective mechanism of PCP on the inflammatory response of PA-induced pulmonary infection model in rats may be through down-regulating the expression of cytokines such as heparin-binding protein and inhibiting the activation of NF-κB and the production of inflammatory factors.
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