Expression and Significance of Na-K-ATPase at Two Sides of Lung Tissues in Rats with Severe Acute Pancreatitis_CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Authors：

Department of Pancreatic Surgery, Shengjing Hospital of China Medical University, Shenyang 110004, Liaoning Province, China;

Corresponding author：

Keywords：

Na-K-ATPase; Severe acute pancreatitis; Alveolar fluid clearance; Pulmonary edema

DOI：

10.7507/1007-9424.20160272

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Objective To discuss the change of expression of Na-K-ATPase mRNA in the rats with severe acute pancreatitis (SAP). Methods Twenty four SPF SD rats were randomly divided into sham group (n=6) and SAP group (n=18), the experiment concluded 3 sub-experiments, and each sub-experiments enrolled 24 rats. After establishment of SAP model successfully, rats of SAP group were randomly divided into SAP-4 h group (n=6), SAP-24 h group (n=6), and SAP-48 h group (n=6). Rats of sham group were only conducted the abdominal exploration. Rats of 4 groups were sacrificed (sham group:4 hours after surgery; SAP-4 h group:4 hours after surgery; SAP-24 h group:24 hours after surgery; SAP-48 h group:48 hours after surgery) to determine the dry/wet ratio, alveolar fluid clearance (AFC), and expressions of Na-K-ATPase mRNA at 2 sides of lung tissues. Results ① Dry/wet ratio. Compared with sham group, the dry/wet ratios of SAP-4 h group, SAP-24 h group, and SAP-48 h group were all lower (P < 0.01); compared with SAP-4 h group, the dry/wet ratio of SAP-24 h group was lower (P < 0.01), but dry/wet ratio of SAP-48 h group was higher (P < 0.01); compared with SAP-24 h group, dry/wet ratio of SAP-48 h group was higher (P < 0.01). ② AFC. Compared with sham group, the AFC value of SAP-4 h group and SAP-24 h group were both higher (P < 0.01), but there was no significant difference between sham group and SAP-48 h group (P > 0.05); compared with SAP-4 h group, the AFC value of SAP-24 h group and SAP-48 h group were both lower (P < 0.01); compared with SAP-24 h group, the AFC value of SAP-48 h group was lower (P < 0.01). ③ α1 Na-K-ATPase mRNA. Compared with corresponding side of lung tissue in sham group, the expression level of α1 Na-K-ATPase mRNA at both 2 sides of lung tissues in SAP-4 h group, SAP-24 h group, and SAP-48 h group were higher (P < 0.01); compared with corresponding side of lung tissue in SAP-4 h group, the expression level of α1 Na-K-ATPase mRNA was lower at left lung tissue (P < 0.05) and was higher at right lung tissue (P < 0.01) in SAP-24 h group, and expression level of α1 Na-K-ATPase mRNA at both sides of lung tissues was lower in SAP-48 h group (P < 0.01); compared with corresponding side of lung tissue in SAP-24 h group, the expression level of α1 Na-K-ATPase mRNA at both 2 sides of lung tissues was lower in SAP-48 h group (P < 0.01). There was no significant difference in the expression level of α1 Na-K-ATPase mRNA between left lung tissue and right lung tissue in sham group, SAP-4 h group, and SAP-48 h group (P > 0.05), but the expression level of α1 Na-K-ATPase mRNA at right lung tissue was higher than that of left lung tissue in SAP-24 h group (P < 0.01). ④ β1 Na-K-ATPase. Compared with corresponding side of lung tissue in sham group, the expression level of β1 Na-K-ATPase mRNA at both 2 sides of lung tissues in SAP-4 h group, SAP-24 h group, and SAP-48 h group was higher (P < 0.01); compared with corresponding side of lung tissue in SAP-4 h group, the expres-sion level of β1 Na-K-ATPase mRNA at both 2 sides of lung tissues in SAP-24 h group was higher (P < 0.01), and lower in right lung tissue of SAP-48 h group (P < 0.01); compared with corresponding side of lung tissue in SAP-24 h group, the expression level of β1 Na-K-ATPase mRNA at both 2 sides of lung tissues was lower in SAP-48 h group (P < 0.01). There was no significant difference in the expression level of β1 Na-K-ATPase mRNA between left lung tissue and right lung tissue in sham group and SAP-48 h group (P > 0.05), but the expression level of β1 Na-K-ATPase mRNA at right lung tissue was higher than that of left lung tissue in SAP-4 h and SAP-24 h group (P < 0.05). Conclusion α1 Na-K-ATPase mRNA may be the key factor for AFC, and may involved in the water transformation in lung tissue of SD rat with SAP.

Citation： XU Jin, LIANG Jie-jia, ZHANG Wei-ming, WANG Hai-nan. Expression and Significance of Na-K-ATPase at Two Sides of Lung Tissues in Rats with Severe Acute Pancreatitis. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2016, 23(9): 1050-1055. doi: 10.7507/1007-9424.20160272 Copy

1.	Pastor CM, Matthay MA, Frossard JL. Pancreatitis-associated acute lung injury-new insights. Chest, 2003, 124(6):2341-2351.
2.	Browne GW, Pitchumoni CS. Pathophysiology of pulmonary complications of acute pancreatitis. World J Gastroenterol, 2006, 12(44):7087-7096.
3.	Zhou MT, Chen CS, Chen BC, et al. Acute lung injury and ARDS in acute pancreatitis:mechanisms and potential intervention. World J Gastroenterol, 2010, 16(17):2094-2099.
4.	Elder AS, Saccone GT, Dixon DL. Lung injury in acute pancreatitis:mechanisms underlying augmented secondary injury. Pancreatology, 2012, 12(1):49-56.
5.	陈芳, 李茹, 李林艳, 等.脂氧素A4对内毒素攻击的肺泡Ⅱ型上皮细胞Na⁺-K⁺-ATP酶的影响.中华急诊医学杂志, 2010, 19(12):1269-1274.
6.	Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis-2012:revision of the Atlanta classification and definitions by international consensus. Gut, 2013, 62(1):102-111.
7.	中华医学会消化病学分会胰腺疾病学组, 中华胰腺病杂志编辑委员会, 中华消化杂志编辑委员会.中国急性胰腺炎诊治指南(2013年, 上海).胃肠病学, 2013, 18(7):428-433.
8.	Vege SS, Gardner TB, Chari ST, et al. Low mortality and high morbidity in severe acute pancreatitis without organ failure:a case for revising the Atlanta classification to include "moderately severe acute pancreatitis". Am J Gastroenterol, 2009, 104(3):710-715.
9.	Giakoustidis A, Mudan SS, Giakoustidis D. Dissecting the stress activating signaling pathways in acute pancreatitis. Hepatogastroenterology, 2010, 57(99-10):653-656.
10.	Matthay MA, Ware LB. Resolution of alveolar edema in acute respiratory distress syndrome. Physiology and biology. Am J Respir Crit Care Med, 2015, 192(2):124-125.
11.	Clerici C. The challenge of modeling human acute respiratory distress syndrome:a new model of lung injury due to sepsis with impaired alveolar edema fluid removal. Am J Physiol Lung Cell Mol Physiol, 2011, 301(1):L20-L22.
12.	Kangelaris KN, Prakash A, Liu KD, et al. Increased expression of neutrophil-related genes in patients with early sepsis-induced ARDS. Am J Physiol Lung Cell Mol Physiol, 2015, 308(11):L1102-L1113.
13.	Gotts JE, Matthay MA. Endogenous and exogenous cell-based pathways for recovery from acute respiratory distress syndrome. Clin Chest Med, 2014, 35(4):797-809.
14.	Gotts JE, Abbott J, Matthay MA. Influenza causes prolonged disruption of the alveolar-capillary barrier in mice unresponsive to mesenchymal stem cell therapy. Am J Physiol Lung Cell Mol Physiol, 2014, 307(5):L395-L406.
15.	Gao Z, Xu J, Sun D, et al. Traditional Chinese medicine, Qing Ying Tang, ameliorates the severity of acute lung injury induced by severe acute pancreatitis in rats via the upregulation of aquaporin-1. Exp Ther Med, 2014, 8(6):1819-1824.
16.	Factor P, Saldias F, Ridge K, et al. Augmentation of lung liquid clearance via adenovirus-mediated transfer of a Na, K-ATPase beta1 subunit gene. J Clin Invest, 1998, 102(7):1421-1430.
17.	Geering K. Functional roles of Na, K-ATPase subunits. Curr Opin Nephrol Hypertens, 2008, 17(5):526-532.
18.	Huynh TP, Barwe SP, Lee SJ, et al. Glucocorticoids suppress renal cell carcinoma progression by enhancing Na, K-ATPase beta-1 subunit expression. PLoS One, 2015, 10(4):e0122442.
19.	Wang C, Ruan R, Zhang L, et al. Role of the Na(+)/K(+)-ATPase beta-subunit in peptide-mediated transdermal drug delivery. Mol Pharm, 2015, 12(4):1259-1267.
20.	Tokhtaeva E, Sachs G, Sun H, et al. Identification of the amino acid region involved in the intercellular interaction between the β1 subunits of Na⁺/K⁺-ATPase. J Cell Sci, 2012, 125(Pt 6):1605-1616.
21.	Emr BM, Roy S, Kollisch-Singule M, et al. Electroporation-mediated gene delivery of Na⁺, K⁺-ATPase, and ENaC subunits to the lung attenuates acute respiratory distress syndrome in a two-hit porcine model. Shock, 2015, 43(1):16-23.
22.	Sznajder JI, Factor P, Ingbar DH. Invited review:lung edema clearance:role of Na(+)-K(+)-ATPase. J Appl Physiol (1985), 2002, 93(5):1860-1866.
23.	Xu J, Wang Z, Ma G, et al. Endogenous catecholamine stimulates alveolar fluid clearance in rats with acute pancreatitis. Respirology, 2009, 14(2):195-202.
24.	徐进, 刘宗剑, 梁含理, 等. β2肾上腺素受体对重症急性胰腺炎大鼠肺脏水清除能力的调节作用.中国普外基础与临床杂志, 2014, 21(11):1391-1395.
25.	徐进, 许维雪, 梁含理, 等. α肾上腺素对重症急性胰腺炎大鼠肺脏水调节能力的研究.中国普外基础与临床杂志, 2016, 23(2):167-171.

1. Pastor CM, Matthay MA, Frossard JL. Pancreatitis-associated acute lung injury-new insights. Chest, 2003, 124(6):2341-2351.
2. Browne GW, Pitchumoni CS. Pathophysiology of pulmonary complications of acute pancreatitis. World J Gastroenterol, 2006, 12(44):7087-7096.
3. Zhou MT, Chen CS, Chen BC, et al. Acute lung injury and ARDS in acute pancreatitis:mechanisms and potential intervention. World J Gastroenterol, 2010, 16(17):2094-2099.
4. Elder AS, Saccone GT, Dixon DL. Lung injury in acute pancreatitis:mechanisms underlying augmented secondary injury. Pancreatology, 2012, 12(1):49-56.
5. 陈芳, 李茹, 李林艳, 等.脂氧素A4对内毒素攻击的肺泡Ⅱ型上皮细胞Na⁺-K⁺-ATP酶的影响.中华急诊医学杂志, 2010, 19(12):1269-1274.
6. Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis-2012:revision of the Atlanta classification and definitions by international consensus. Gut, 2013, 62(1):102-111.
7. 中华医学会消化病学分会胰腺疾病学组, 中华胰腺病杂志编辑委员会, 中华消化杂志编辑委员会.中国急性胰腺炎诊治指南(2013年, 上海).胃肠病学, 2013, 18(7):428-433.
8. Vege SS, Gardner TB, Chari ST, et al. Low mortality and high morbidity in severe acute pancreatitis without organ failure:a case for revising the Atlanta classification to include "moderately severe acute pancreatitis". Am J Gastroenterol, 2009, 104(3):710-715.
9. Giakoustidis A, Mudan SS, Giakoustidis D. Dissecting the stress activating signaling pathways in acute pancreatitis. Hepatogastroenterology, 2010, 57(99-10):653-656.
10. Matthay MA, Ware LB. Resolution of alveolar edema in acute respiratory distress syndrome. Physiology and biology. Am J Respir Crit Care Med, 2015, 192(2):124-125.
11. Clerici C. The challenge of modeling human acute respiratory distress syndrome:a new model of lung injury due to sepsis with impaired alveolar edema fluid removal. Am J Physiol Lung Cell Mol Physiol, 2011, 301(1):L20-L22.
12. Kangelaris KN, Prakash A, Liu KD, et al. Increased expression of neutrophil-related genes in patients with early sepsis-induced ARDS. Am J Physiol Lung Cell Mol Physiol, 2015, 308(11):L1102-L1113.
13. Gotts JE, Matthay MA. Endogenous and exogenous cell-based pathways for recovery from acute respiratory distress syndrome. Clin Chest Med, 2014, 35(4):797-809.
14. Gotts JE, Abbott J, Matthay MA. Influenza causes prolonged disruption of the alveolar-capillary barrier in mice unresponsive to mesenchymal stem cell therapy. Am J Physiol Lung Cell Mol Physiol, 2014, 307(5):L395-L406.
15. Gao Z, Xu J, Sun D, et al. Traditional Chinese medicine, Qing Ying Tang, ameliorates the severity of acute lung injury induced by severe acute pancreatitis in rats via the upregulation of aquaporin-1. Exp Ther Med, 2014, 8(6):1819-1824.
16. Factor P, Saldias F, Ridge K, et al. Augmentation of lung liquid clearance via adenovirus-mediated transfer of a Na, K-ATPase beta1 subunit gene. J Clin Invest, 1998, 102(7):1421-1430.
17. Geering K. Functional roles of Na, K-ATPase subunits. Curr Opin Nephrol Hypertens, 2008, 17(5):526-532.
18. Huynh TP, Barwe SP, Lee SJ, et al. Glucocorticoids suppress renal cell carcinoma progression by enhancing Na, K-ATPase beta-1 subunit expression. PLoS One, 2015, 10(4):e0122442.
19. Wang C, Ruan R, Zhang L, et al. Role of the Na(+)/K(+)-ATPase beta-subunit in peptide-mediated transdermal drug delivery. Mol Pharm, 2015, 12(4):1259-1267.
20. Tokhtaeva E, Sachs G, Sun H, et al. Identification of the amino acid region involved in the intercellular interaction between the β1 subunits of Na⁺/K⁺-ATPase. J Cell Sci, 2012, 125(Pt 6):1605-1616.
21. Emr BM, Roy S, Kollisch-Singule M, et al. Electroporation-mediated gene delivery of Na⁺, K⁺-ATPase, and ENaC subunits to the lung attenuates acute respiratory distress syndrome in a two-hit porcine model. Shock, 2015, 43(1):16-23.
22. Sznajder JI, Factor P, Ingbar DH. Invited review:lung edema clearance:role of Na(+)-K(+)-ATPase. J Appl Physiol (1985), 2002, 93(5):1860-1866.
23. Xu J, Wang Z, Ma G, et al. Endogenous catecholamine stimulates alveolar fluid clearance in rats with acute pancreatitis. Respirology, 2009, 14(2):195-202.
24. 徐进, 刘宗剑, 梁含理, 等. β2肾上腺素受体对重症急性胰腺炎大鼠肺脏水清除能力的调节作用.中国普外基础与临床杂志, 2014, 21(11):1391-1395.
25. 徐进, 许维雪, 梁含理, 等. α肾上腺素对重症急性胰腺炎大鼠肺脏水调节能力的研究.中国普外基础与临床杂志, 2016, 23(2):167-171.

CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Expression and Significance of Na-K-ATPase at Two Sides of Lung Tissues in Rats with Severe Acute Pancreatitis

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