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
Abstract
Minli Li, Ren-Min Zhu, Xiaohua Zhang, Jingyun Guo, Miaofang Yang, Xiaowei Wu, Guo Meixia
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.
OpenAlex reports 3 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
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