2011Jiefangjun yixue zazhiRequires access

The role of JAK2/STAT3 signaling pathway in the lung injury rat with severe acute pancreatitis

Minli Li, Ren-Min Zhu, Xiaohua Zhang, Jingyun Guo, Miaofang Yang, Xiaowei Wu, Guo Meixia

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Abstract

Objective To investigate the mechanism of action of JAK/STAT signaling pathways in the lung injury of experimental severe acute pancreatitis(SAP).Methods The rat model of SAP was reproduced by retrograde injection of 4% sodium taurocholate into the biliopancreatic duct.Thirty-two male SD rats were randomly assigned into 4 groups(8 each): normal control group(NC),SAP 6h,12h and 18h groups.The level of serum amylase(AMY) was measured dynamically.The pathological changes in pancreas and lung were observed under the light microscope,and the wet/dry weight ratios of lung were evaluated.The concentrations of IL-6 and IL-18 were determined by ELISA,and the expressions of JAK2 and STAT3 protein in lung were determined by Western blotting.Results Compared with NC group,serum level of AMY increased significantly in SAP groups(P < 0.01),and the pancreas and lung injuries under the light microscope were gradually aggravated with disease progression.The wet/dry weight ratio of lung in SAP groups increased significantly compared with that in NC group(P < 0.01).The serum concentrations of IL-6,IL-18 in the SAP groups increased significantly compared with those in NC group(P < 0.01).The concentrations of JAK2 and STAT3 protein in SAP groups increased significantly compared with that in NC group(P < 0.01) and reached the peak in 12-18 hours.Conclusion Activation of JAK2/STAT3 signaling pathways may induce the over-expressions of IL-6 and IL-18,and aggravate the inflammatory reaction and lung injury induced by SAP.

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Objective To investigate the mechanism of action of JAK/STAT signaling pathways in the lung injury of experimental severe acute pancreatitis(SAP).Methods The rat model of SAP was reproduced by retrograde injection of 4% sodium taurocholate into the biliopancreatic duct.Thirty-two male SD rats were randomly assigned into 4 groups(8 each): normal control group(NC),SAP 6h,12h and 18h groups.The level of serum amylase(AMY) was measured dynamically.The pathological changes in pancreas and lung were observed under the light microscope,and the wet/dry weight ratios of lung were evaluated.The concentrations of IL-6 and IL-18 were determined by ELISA,and the expressions of JAK2 and STAT3 protein in lung were determined by Western blotting.Results Compared with NC group,serum level of AMY increased significantly in SAP groups(P < 0.01),and the pancreas and lung injuries under the light microscope were gradually aggravated with disease progression.The wet/dry weight ratio of lung in SAP groups increased significantly compared with that in NC group(P < 0.01).The serum concentrations of IL-6,IL-18 in the SAP groups increased significantly compared with those in NC group(P < 0.01).The concentrations of JAK2 and STAT3 protein in SAP groups increased significantly compared with that in NC group(P < 0.01) and reached the peak in 12-18 hours.Conclusion Activation of JAK2/STAT3 signaling pathways may induce the over-expressions of IL-6 and IL-18,and aggravate the inflammatory reaction and lung injury induced by SAP.

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Available abstract

Objective To investigate the mechanism of action of JAK/STAT signaling pathways in the lung injury of experimental severe acute pancreatitis(SAP).Methods The rat model of SAP was reproduced by retrograde injection of 4% sodium taurocholate into the biliopancreatic duct.Thirty-two male SD rats were randomly assigned into 4 groups(8 each): normal control group(NC),SAP 6h,12h and 18h groups.The level of serum amylase(AMY) was measured dynamically.The pathological changes in pancreas and lung were observed under the light microscope,and the wet/dry weight ratios of lung were evaluated.The concentrations of IL-6 and IL-18 were determined by ELISA,and the expressions of JAK2 and STAT3 protein in lung were determined by Western blotting.Results Compared with NC group,serum level of AMY increased significantly in SAP groups(P < 0.01),and the pancreas and lung injuries under the light microscope were gradually aggravated with disease progression.The wet/dry weight ratio of lung in SAP groups increased significantly compared with that in NC group(P < 0.01).The serum concentrations of IL-6,IL-18 in the SAP groups increased significantly compared with those in NC group(P < 0.01).The concentrations of JAK2 and STAT3 protein in SAP groups increased significantly compared with that in NC group(P < 0.01) and reached the peak in 12-18 hours.Conclusion Activation of JAK2/STAT3 signaling pathways may induce the over-expressions of IL-6 and IL-18,and aggravate the inflammatory reaction and lung injury induced by SAP.

Key concepts: Acute pancreatitis, Lung, Medicine, Internal medicine, Pancreas, Endocrinology, Pancreatitis, STAT3

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