Effect of Mogrol on Lung Injury in Rats with Severe Acute Pancreatitis via Cell Pyroptosis Mediated by TREM-1/NLRP3 Pathway
Objective To investigate the effect of mogrol on lung injury in rats with severe acute pancreatitis and its possible mechanism.Methods The model of lung injury in rats with severe acute pancreatitis was established by retrograde injection of 4%sodium taurocholate into the biliopancreatic duct,After modeling,they were divided into model group,mogrol low,medium and high dose groups(15,30,60 mg·kg-1),set up another sham operation group,each group containing 12 rats.Intraperitoneal injection,one day once time,a total of 2 times.The pathological changes of pancreas and lung tissues were detected by HE staining;Serum amylase(AMS)and lipase(LPS)levels were detected by biochemical method;The levels of inflammatory cytokines interleukin-1β(IL-1β),interleukin-18(IL-18)and tumor necrosis factor-α(TNF-α)in rat alveolar lavage fluid were determined by ELISA;The activity of Caspase-1 in lung tissue of rats was detected by colorimetry;The expression levels of triggering receptor 1(TREM-1)and pyroptosis related proteins NLRP3,Caspasse-1,Gasdermin D(GSDMD)in lung tissue of rats were detected by Western blot.Results Compared with the sham operation group,the model group showed obvious pathological damage in pancreas and lung tissue.Serum AMS and LPS levels,inflammatory factors IL-1β,IL-18 and TNF-α levels,Caspase-1 activity,and protein expression levels of TREM-1 and NLRP3,Caspasse-1,GSDMD,in lung tissue were significantly increased(P<0.05);Compared with the model group,different doses of mogrol could improve the pathological damage of pancreas and lung tissue in rats,and significantly reduce the levels of serum AMS,LPS,inflammatory factors IL-1β,IL-18 and TNF-α,Caspase-1 activity and the expression levels of TREM-1 and NLRP3,Caspasse-1,GSDMD in lung tissue.Conclusion Mogrol may improve lung injury in rats with severe acute pancreatitis by inhibiting pyroptosis,and its mechanism may be related to the regulation of TREM-1/NLRP3 signaling pathway.
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