Abstract：Objective To investigate the effect of rosiglitazone on oxidative stress in rats with severe acute pancreatitis.Methods Sixty male SD rats were randomly divided into 3 group(n=20): sham operation group (SO group), severe acute pancreatitis group(SAP group) and rosiglitazone treatment group (ROSI group). SAP model was induced by retrograde infusion of 5% sodium taurocholate into the biliopancreatic duct. The rats in ROSI group were injected rosiglitazone(6 mg/kg) throngh femoral vein 5 minutes after the operation. In SO group and SAP group saline partes equales were injected. Rats were killed at 12 h after operation. Analysis of the mortality of rats in each group was conducted. Detecting amylase(AMY), nitric oxide(NO), malondialdehyde(MDA)、glutathione peroxidase(GSH-Px), pancreas pathologic score. Enzyme-linked immunosorbent assay (ELISA)and analysis of serum interleukine-1β (IL-1β), interleukine-6 (IL-6) levels were carried out. The expression of inducible nitric oxide synthase(iNOS)、endothelial nitric oxide synthase(eNOS)in pancreas tissue were measured by Western blotting method.Results Two rats died in SAP group, no rat died in SO group and ROSI group. Compared with SO group, the levels of AMY, NO, MDA and pancreas pathologic score were significantly increased in SAP group.The level of GSH-Px activity decreased significantly in SAP group than in SO group[(39.93±15.18) vs (59.81±22.43) U/mg], which was higher in ROSI group than in SAP group[(49.01±9.42) vs (59.81±22.43) U/mg] (P<0.05). The expression of iNOS and eNOS in pancreas tissue increased significantly in SAP group than in SO group[(1.90±0.16) vs (0.75±0.09),(0.37±0.09) vs (0.09±0.01)] (P<0.05); compared with SAP group, these indexes decreased significantly in ROSI group[(1.31±0.18) vs (1.90±0.16)、(0.23±0.08) vs (0.37±0.09)] (P<0.05).Conclusions Rosiglitazone exerts the protective effect on severe acute pancreatitis through inhibiting oxidative stress and downregulating the expression of inflammatory cytokine.
Banks P A, Bollen T L, Dervenis C, et al. Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus[J]. Gut, 2013,62(1):102-111.
[2]
Wang G, Qu F Z, Li L, et al. Necroptosis: a potential, promising target and switch in acute pancreatitis[J]. Apoptosis, 2016, 21(2):121-129.
[3]
Pérez S, Pereda J, Sabater L, et al. Redox signaling in acute pancreatitis[J]. Redox Biol, 2015, 5:1-14.
[4]
Chen C, Xu S, Wang W X, et al. Rosiglitazone attenuates the severity of sodium taurocholate-induced acute pancreatitis and pancreatitis-associated lung injury[J]. Arch Med Res,2009,40(2):79-88.
Schmidt J, Rattner D W, Lewandrowski K, et al. A better model of acute pancreatitis for evaluating therapy[J]. Ann Surg, 1992, 215(1):44-56.
[7]
Wang G J, Gao C F, Wei D, et al. Acute pancreatitis: etiology and common pathogenesis[J]. World J Gastroenterol, 2009, 15(12):1427-1430.
[8]
Quinlan J D. Acute pancreatitis[J]. Am Fam Physician, 2014, 90(9):632-639.
[9]
Yu J H, Kim H. Oxidative stress and inflammatory signaling in cerulein pancreatitis [J]. World J Gastroenterol, 2014, 20(46):17324-17329.
[10]
Chaudhari N, Talwar P, Parimisetty A, et al. A molecular web: endoplasmic reticulum stress, inflammation, and oxidative stress[J]. Front Cell Neurosci, 2014, 8:213.
[11]
Sinha K, Das J, Pal P B, et al. Oxidative stress: the mitochondria-dependent and mitochondria-independent pathways of apoptosis[J]. Arch Toxicol,2013,87(7):1157-1180.
[12]
Dizdaroglu M. Oxidatively induced DNA damage: mechanisms, repair and disease[J]. Cancer Lett, 2012, 327(1-2):26-47.
[13]
Zhu L, Yuan H, Guo C, et al. Zearalenone induces apoptosis and necrosis in porcine granulosa cells via a caspase-3- and caspase-9-dependent mitochondrial signaling pathway[J]. J Cell Physiol, 2012, 227(5):1814-1820.
[14]
Lee H, Jeon J, Ryu Y S, et al. Disruption of microtubules sensitizes the DNA damage-induced apoptosis through inhibiting nuclear factor kappaB (NF-kappaB) DNA-binding activity[J]. J Korean Med Sci,2010,25(11):1574-1581.
[15]
Wagner M C, Yeligar S M, Brown L A, et al. PPARγ ligands regulate NADPH oxidase, eNOS, and barrier function in the lung following chronic alcohol ingestion[J]. Alcohol Clin Exp Res, 2012, 36(2):197-206.
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