RESUMEN
To study the effect of oral lienal polypeptide on cough and inflammation in mice, in order to expand the clinical application of immune modulator lienal polypeptide and provide a new strategy for relieving cough and inflammation. METHODS: The cough model of mice was induced by concentrated ammonia. The cough frequency and tolerance latency of mice within 6 minutes were recorded every day. The histopathological changes of spleen and lung were evaluated by HE staining and spleen index. TNF-α, IL-1β and IL-6 levels in spleen and lung of mice was detected by ELISA. RESULTS: Oral administration of spleen polypeptide could prolong the tolerance latency of mice to concentrated ammonia to a certain extent and significantly reduce the cough frequency of mice. HE staining showed that oral spleen polypeptide could significantly reduce the alveolar surface area and improve lung expansion in mice. The results of ELISA showed that oral spleen polypeptide decreased the levels of some proinflammatory factors in spleen and lung. CONCLUSION: Lienal polypeptide can alleviate cough and emphysema like symptoms induced by ammonia, improve immune ability and inflammation in mice.
RESUMEN
Objective:To investigate the role and mechanism of leptin on dendritic cells by NLRP3 inflammasome.Methods: BMDCs were induced in vitro,leptin with scalar doses was cocultured with BMDCs,IL-1β and IL-18 mRNA expression and protein secretion level were measured by q-RT-PCR and ELISA respectively.Caspase-1 activity or ROS synthesis were tested with FLICA kit or ROS detection assay kit on flow cytometry.IL-1β or IL-18 were detected after caspase-1 was inhibited by Ac-YVAD-cmk or NLRP3 was interfered by siRNA or ROS inhibitor DPI or KCL were added.Results: Leptin promoted secretion of IL-1β and IL-18.Leptin up-regulated NLRP3 and activted caspase-1 to secret proinflammtory cytokine,which K+ efflux took part in.Conclusion: Leptin promotes secretion of IL-1β and IL-18 by activating NLRP3 inflammasome,and K+ efflux takes part in this,which hints us that leptin may be an activator of NLRP3 inflammasome.