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

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7.	中華醫學會消化病學分會胰腺疾病學組, 中華胰腺病雜志編輯委員會, 中華消化雜志編輯委員會.中國急性胰腺炎診治指南(2013年, 上海).胃腸病學, 2013, 18(7):428-433.
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9.	Giakoustidis A, Mudan SS, Giakoustidis D. Dissecting the stress activating signaling pathways in acute pancreatitis. Hepatogastroenterology, 2010, 57(99-10):653-656.
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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.	徐進, 劉宗劍, 梁含理, 等. β2腎上腺素受體對重癥急性胰腺炎大鼠肺臟水清除能力的調節作用.中國普外基礎與臨床雜志, 2014, 21(11):1391-1395.
25.	徐進, 許維雪, 梁含理, 等. α腎上腺素對重癥急性胰腺炎大鼠肺臟水調節能力的研究.中國普外基礎與臨床雜志, 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. 陳芳, 李茹, 李林艷, 等.脂氧素A4對內毒素攻擊的肺泡Ⅱ型上皮細胞Na⁺-K⁺-ATP酶的影響.中華急診醫學雜志, 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. 中華醫學會消化病學分會胰腺疾病學組, 中華胰腺病雜志編輯委員會, 中華消化雜志編輯委員會.中國急性胰腺炎診治指南(2013年, 上海).胃腸病學, 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. 徐進, 劉宗劍, 梁含理, 等. β2腎上腺素受體對重癥急性胰腺炎大鼠肺臟水清除能力的調節作用.中國普外基礎與臨床雜志, 2014, 21(11):1391-1395.
25. 徐進, 許維雪, 梁含理, 等. α腎上腺素對重癥急性胰腺炎大鼠肺臟水調節能力的研究.中國普外基礎與臨床雜志, 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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