Correlation Of IL-33Expression And Inflammatory Mediators In Acute Pancreatitis

Objective:To investigate the relationship between IL-33expression in acute pancreatitis, as wellas inflammatory mediators and analysis of IL-33in acute pancreatitis in the role ofpro-inflammatory mechanisms and signal transduction pathways for the clinical diagnosisof acute pancreatitis and therapy molecular mechanisms.Methods：The clinical diagnosis of acute pancreatitis patients collected60cases and30cases ofnormal healthy control samples, testing of all specimens of IL-33using enzyme-linkedimmunosorbent assay (ELISA), sST2, TNF-α, IL-6and serum biochemistry indicators andwith patients Ranson score, APACHE II score line correlation analysis, observation andclinical significance of the relationship between the indexes. Establishment of rat model ofacute pancreatitis, as control sham group, each group were observed in rat pancreatic4,8,12,24h pathological changes in rat pancreas and blood collection,immunohistochemis-try;enzyme-linked immuneosorbent assay (ELISA) in each group at different times ofserum IL-33, sST2, TNF-α, IL-6and serum biochemical changes in the indicators;REAL-TIME PCR method and WESTERN-BLOT assay in each group at different timepancreatic tissue IL-33, the expression of ST2, the dynamic relationship between theexpression was observed in rat model of acute pancreatitis in IL-33at different times andamong various inflammatory mediators, analyze the role of IL-33in patients with acutepancreatitis.Results：Serum of patients with acute pancreatitis, IL-33, TNF-α, IL-6expression were higherthan normal controls, serum sST2expression decreased, the gap is statistically significant(P <0.05); expression of IL-33and TNF-α, IL-6was positively correlated with sST2 negatively correlated statistically significant difference (P <0.05); IL-33expression inpatients with Ranson score, APACHE II score positively correlated. Acute pancreatitis inrats8h, surgery group of IL-33, TNF-α, IL-6were elevated compared with the controlgroup, sST2lower than the control group, the difference was statistically significant(P<0.05), and IL-33expression and pathological score, TNF-α, IL-6expression positivelycorrelated with sST2negative correlation;8h IL-33expression after the surgery groupdecreased, no significant difference (P>0.05)24h with the control group; pancreatictissue mRNA and protein levels have IL-33, ST2expression, and is consistent withchanges in serum, immunohistochemistry confirmed changes in rats with acutepancreatitis.Conclusion:1. IL-33is over-expression in acute pancreatitis, and the expression of IL-33isassociated with inflammatory mediators such as sST2, TNF-α, IL-6and Ranson score,APACHE II score of the patients.2. IL-33is over-expression in rat model of acute pancreatitis, and the expression ofIL-33is associated with inflammatory mediators such as sST2, TNF-α, IL-6.3. IL-33has a role in promoting the expression of inflammatory mediators, mayplay an active role in the inflammatory response in acute pancreatitis.