吡格列酮对重症急性胰腺炎血清细胞因子和组织病理学评分的影响

目的探讨TNF-α、IL-6和IL-10在大鼠重症急性胰腺炎（SAP）早期的动态变化及意义,并观察吡格列酮的干预性作用。方法将54只雄性SD大鼠随机分成假手术组（C组）、SAP组、吡格列酮组（P组）。采用逆行胰胆管注射法建立SAP模型;P组大鼠在造模前2h腹腔内注射吡格列酮溶液50mg/kg。于造模后3h、6h、12h分批处死大鼠,采用全自动生化分析仪检测血清淀粉酶;ELISA法检测血清TNF-α、IL-6、IL-10的含量;并常规HE染色进行胰腺组织病理学评分。结果 SAP组与C组比较,胰腺组织病理评分、血清淀粉酶、TNF-α及IL-6含量在各时间点均升高（P〈0.01）,IL-10含量无统计学意义（P〉0.05）;干预性使用吡格列酮后,胰腺组织病理学评分、血清淀粉酶、TNF-α及IL-6水平与SAP组相比均有降低（P〈0.05）,IL-10水平高于SAP组（P〈0.05）。结论在SAP早期阶段细胞因子的变化与病情进展密切相关,吡格列酮可通过调节促炎与抗炎因子的平衡,减轻炎症反应。

Dynamic changes of cytokines and the effect of pioglitazone on them in early stage of severe acute pancreatitis

Objective To observe the dynamic changes and significances of TNF-α,IL-6 and IL-10 in severe acute pancreatitis （SAP） rats,and assess the effect of pretreatment with pioglitazone on them.Methods 54 male Sprague-Dawley（SD） rats were randomly divided into sham group（C group）,SAP group,and pioglitazone group（P group）.（1） SAP group was induced by the retrograde injection of sodium taurocholate （STC） in the pancreatic duct （n=18） ;（2） P group （same as SAP group,but pioglitazone （50 mg/kg） was injected intraperitoneally two hours prior to STC（n=18） ;（3） Sham operation group.Sham-operated animals served as control.Operation was executed,STC was not injected,but pancreas was flipped and striked gently three times.Rats were killed by abdominal aorta exsanguination at 3 h,6 h and 12 h after the induction of pancreatitis.Serum activities of amylase were measured,the concentrations of inflammatory cyctokines （TNF-α,IL-6 and IL-10） of the blood were measured by ELISA and pancreatic histologic score were assessed.Results Compared with C group,pancreatic histologic score,serum amylase,TNF-α and IL-6 in SAP group were increased significantly （P 〈 0.01） except IL-10 level （P 〉0.05）.Pretreatment with pioglitazone obviously decreased histologic score and the serum level of amylase,TNF-α,IL-6,and the level of IL-10 was higher than SAP group in early SAP （P 〈 0.05）.Conclusions Cytokines play an important role in early progress of SAP;pioglitazone could attenuate the severity of inflammatory response through regulating the balance of pro-and anti-inflammatory cytokines.