Department of Gastroenterology, Branch Hospital of the First People's Hospital, Shanghai Jiao Tong University, School of Medicine, 201600, Shanghai, China.
Dig Dis Sci. 2011 Apr;56(4):1082-9. doi: 10.1007/s10620-010-1393-0. Epub 2010 Sep 8.
Studies suggest that peroxisome proliferator-activated receptor γ(PPARγ) ligands may represent a therapeutic option in acute pancreatitis, yet most of them have been prophylactic administrated.
To evaluate the therapeutic effect of pioglitazone in rats with severe acute pancreatitis induced by sodium taurocholate.
Severe acute pancreatitis (SAP) was induced in male Sprague-Dawley rats by the retrograde injection of 5% sodium taurocholate into the pancreatic duct. After SAP was induced, pioglitazone was injected intraperitoneally and its role on the severity of inflammatory response and pancreatic injury was investigated. Amylase activity, inflammatory cytokines production, pathological changes of pancreas, PPARγ mRNA expression, and the survival rate were examined.
Treatment with pioglitazone decreased the level of amylase activity, proinflammatory factors IL-6 and TNF-α, ameliorated pancreatic histological score, and upregulated the expression of PPARγ mRNA. The survival rate in the early stage of severe acute pancreatitis was also improved.
Pioglitazone can be used as a therapeutic drug and relieve the damages caused by SAP, which suggests PPARγ ligand-pioglitazone offers a potent approach for the treatment of severe acute pancreatitis.
研究表明过氧化物酶体增殖物激活受体γ（PPARγ）配体可能是急性胰腺炎的一种治疗选择，但它们大多数都是预防性给药。
评估吡格列酮在牛磺胆酸钠诱导的大鼠重症急性胰腺炎中的治疗作用。
雄性 Sprague-Dawley 大鼠通过逆行胰管注射 5%牛磺胆酸钠诱导重症急性胰腺炎（SAP）。SAP 诱导后，腹腔内注射吡格列酮，观察其对炎症反应和胰腺损伤严重程度的影响。检测淀粉酶活性、炎症细胞因子的产生、胰腺的病理变化、PPARγmRNA 表达和存活率。
吡格列酮治疗降低了淀粉酶活性、促炎因子 IL-6 和 TNF-α 的水平，改善了胰腺组织学评分，并上调了 PPARγmRNA 的表达。重症急性胰腺炎早期的存活率也得到了提高。
吡格列酮可作为一种治疗药物，减轻 SAP 引起的损伤，这表明 PPARγ 配体吡格列酮为治疗重症急性胰腺炎提供了一种有效的方法。
