JAK2-STAT3信号通路在重症急性胰腺炎大鼠肺组织中表达与外周炎性因子的相关性

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Abstract Objective To investigate expression of JAK2-STAT3 signaling pathway in lung tissues of rats with severe acute pancreatitis (SAP) and its correlation with peripheral inflammatory factors. Methods 5-month-old male Wistar rats (n = 240) were randomly divided into SAP group, SAP+R group, SAP+S group, SAP+R+S group and sham-operated group (SO group), 48 rats in each group. Abdominal aortic blood and lung tissues were collected 3, 6, 12 and 18 hours after model establishment in each group animals. Serum interleukin-6 (IL-6) and interleukin-10 (IL-10) were measured. The expression levels of JAK2 mRNA, STAT3 mRNA, p-JAK2 Protein and p-STAT3 protein in lung tissues were detected. Results The levels of serum IL-6 and IL-10 at 3, 6, 12 and 18 hours after model establishment were significantly different among the five groups (P < 0.05). There was significant difference in serum IL-10 level in SO group (P < 0.05). The serum levels of IL-6 and IL-10 in SAP group, SAP+R group, SAP+S group and SAP+R+S group increased gradually at 3 hours after model establishment, peaked at 12 hours after model establishment, and then decreased, there were statistically significant differences among different time points with in the group (P < 0.05). The expression levels of JAK2 mRNA, STAT3 mRNA, p-JAK2 protein and p-STAT3 protein in lung tissue of five groups at 3, 6, 12 and 18 hours after model establishment were significantly different (P < 0.05). The expression levels of JAK2 mRNA, STAT3 mRNA, p-JAK2 protein and p-STAT3 protein protein in lung tissues of five groups increased gradually at 3 hours after model establishment, peaked at 12 hours after model establishment, and then decreased, there were statistically significant differences among different time points within groups (P < 0.05). Conclusion Activation of JAK2/STAT3 pathway may be closely related to systemic inflammatory response in the course of SAP.

Key words： Severe acute pancreatitis JAK2-STAT3 signaling pathway Lung tissue Inflammatory factors

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	SHEN Yinfeng JIN Wenyin ZHANG Xia CHEN Qian

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SHEN Yinfeng JIN Wenyin ZHANG Xia CHEN Qian. Expression of JAK2-STAT3 signaling pathway in lung tissues of rats with severe acute pancreatitis and its correlation with peripheral inflammatory factors[J]. 中国医药导报, 2019, 16(26): 17-21.

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http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2019/V16/I26/17

[1] Bumbasirevic V，Radenkovic D，Jankovic Z，et al. Severe acute pancreatitis：overall and early versus late mortality in intensive care units [J]. Pancreas，2009，38（2）：122-125.
[2] Polyzogopoulou E， Bikas C，Danikas D，et al. Baseline hypoxemia as a prognostic marker for pulmonary complications and outcome in patients with acute pancreatitis [J]. Dig Dis Sci，2004，49（1）：150-154.
[3] Wang G，Zhang J，Xu C，et al. Inhibition of SOCs attenuates acute lung injury induced by severe acute pancreatitis in Rats and PMVECs injury induced by lipopolysaccharide [J]. Inflammation，2016，39（3）：1049-1058.
[4] Shen Y，Cui N，Miao B，et al. Immune dysregulation in patients with severe acute pancreatitis [J]. Inflammation，2011，34（1）：36-42.
[5] Chan YC，Leung PS. Acute pancreatitis：animal models and recent advances in basic research [J]. Pancreas，2007，34（1）：1-14.
[6] Liongue C，Ward AC. Evolution of the JAK-STAT pathway [J]. Jakstat，2013，2：e22756.
[7] Aho HJ，Ahola RA，Tolvanen AM，et al. Experimental pancreatitis in the rat changes in pulmonary phospholipids during sodium taurocholate-induced acute pancreatitis [J]. Res Exp Med （Berl），1983，182（1）：79-84.
[8] Browne GW，Pitchumoni CS. Pathophysiology of pulmonary complications of acute pancreatitis [J]. World J Gastroenterol，2006，12（44）：7087-7096.
[9] Zhang L，Nie Y，Zheng Y，et al. Esmolol attenuates lung injury and inflammation in severe acute pancreatitis rats [J]. Pancreatology, 2016，16（5）：726-732.
[10] Ma P，Yu K，Yu J，et al. Effects of nicotine and vagus nerve in severe acute pancreatitis-associated lung injury in rats [J]. Pancreas，2016，45（4）：552-560.
[11] Bryniarski K，Maresz K，Szczepanik M，et al. Modulation of macrophage activity by proteolytic enzymes. Differential regulation of IL-6 and reactive oxygen intermediates （ROIs） synthesis as a possible homeostatic mechanism in the control of inflammation [J]. Inflammation，2003，27（6）：333-340.
[12] Bendicho MT，Guedes JC，Silva NN，et al. Polymorphism of cytokine genes （TGF-beta1，IFN-gamma，IL-6，IL-10，and TNF-alpha） in patients with chronic pancreatitis [J]. Pancreas，2005，30（4）：333-336.
[13] O′Sullivan LA，Liongue C，Lewis RS，et al. Cytokine receptor signaling through the Jak-Stat-Socs pathway in disease [J]. Mol Immunol，2007，44：2497-2506.
[14] Stepkowski SM，Chen W，Ross JA，et al. STAT3：an important regulator of multiple cytokine functions [J]. Transplantation，2008，85（10）：1372-1377.
[15] Verstovsek S. Ruxolitinib：an oral Janus kinase 1 and Janus kinase 2 inhibitor in the management of myelofibrosis [J]. Postgrad Med，2013，125（1）：128-135.
[16] Schust J，Sperl B，Hollis A，et al. Stattic：a small-molecule inhibitor of STAT3 activation and dimerization [J]. Chem Biol，2006，13（11）：1235-1242.
[17] Yu JH，Kim H. Role of janus kinase/signal transducers and activators of transcription in the pathogenesis of pancreatitis and pancreatic cancer [J]. Gut Liver，2012，6（4）：417-422.
[18] Zhu S，Zhang C，Weng Q，et al. Curcumin protects against acute renal injury by suppressing JAK2/STAT3 pathway in severe acute pancreatitis in rats [J]. Exp Ther Med，2017，14（2）：1669-1674.
[19] Han X，Wang Y，Chen H，et al. Enhancement of ICAM-1 via the JAK2/STAT3 signaling pathway in a rat model of severe acute pancreatitis-associated lung injury [J]. Exp Ther Med，2016，11（3）：788-796.
[20] 徐志红，白永愉，黄新策，等.垂盆草提取物经JAK2/STAT3信号通路途径改善大鼠重症急性胰腺炎肺损伤的研究[J].肝胆胰外科杂志，2014，26（5）：398-402.