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Evidence-Based Complementary and Alternative Medicine Volume 2019 ,2019-07-15
Keratinocyte Growth Factor-2 Is Protective in Oleic Acid-Induced Acute Lung Injury in Rats
Research Article
S. Tenghao 1 , 2 M. Shenmao 3 W. Zhaojun 1 B. Jijia 1 Z. Wenjie 1 Z. Wenyan 1 M. Xigang 1
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DOI:10.1155/2019/9406580
Received 2019-04-09, accepted for publication 2019-05-26, Published 2019-05-26
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摘要

Objective. The aim of this study was to examine the role of keratinocyte growth factor-2 (KGF-2) in oleic acid-induced acute lung injury (ALI) in rats. Methods. Forty-five healthy adult male Sprague Dawley rats were divided into 3 groups. Rat ALI model was established by injection of 0.01 mL/kg oleic acid into the tail vein. Rats in the control group were injected with the same amount of normal saline (NS). In the ALI + KGF-2 group, 5 mg/kg of KGF-2 was instilled into the airway of rats 72 hours before the model preparation, and the control group and the ALI model group were instilled with the same amount of NS. The lung permeability index (LPI) and lung wet/dry weight (W / D) ratios were measured 8 hours after the model preparation. The permeability of pulmonary microvascular endothelium was evaluated by Evans blue leakage test. Histopathological changes were observed under light microscope and the ALI pathology score (LIS) was calculated. Ultrastructural changes of lung tissue were observed under electron microscope. The apoptosis was detected by TUNEL assay. The expression of Claudin-5, ZO-1, and VE Cadherin in lung tissue was qualitatively and quantitatively analyzed by immunohistochemistry, Western Blot, and qRT-PCR, respectively. Results. The ALI model group had severe lung injury and obvious pathological changes, including alveolar septal thickening and inflammatory cell infiltration. TUNEL assay showed that the apoptosis of ALI group was significantly increased. The LIS score, lung W/D ratio, LPI, and Evans blue leakage were significantly higher than those in the control group; electron microscopy showed that the alveolar-capillary barrier was severely damaged in the ALI group. Compared with the control group, the expression of Claudin-5, ZO-1, and VE cadherin in the lung tissue of the ALI model group was significantly attenuated. After pretreatment with KGF-2, the degree of lung tissue damage was significantly reduced and the pathological changes were significantly improved. TUNEL assay showed that the apoptosis of ALI group was decreased. Lung W/D ratio, LPI, and Evans blue leakage decreased; electron microscopy showed that the alveolar-capillary barrier of ALI group recovered significantly. Compared with the ALI model group, the expression of Claudin-5, ZO-1, and VE cadherin in the lung tissue of the KGF-2 pretreatment group increased. Conclusion. The results indicate that KGF-2 may attenuate oleic acid-induced ALI in rats by maintaining the pulmonary microvascular endothelial barrier, which is an effective ALI preventive measure.

授权许可

Copyright © 2019 S. Tenghao et al. 2019
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

通讯作者

M. Xigang.Department of Critical Care Medicine, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, China, nxmu.edu.cn.nyfyicu@163.com

推荐引用方式

S. Tenghao,M. Shenmao,W. Zhaojun,B. Jijia,Z. Wenjie,Z. Wenyan,M. Xigang. Keratinocyte Growth Factor-2 Is Protective in Oleic Acid-Induced Acute Lung Injury in Rats. Evidence-Based Complementary and Alternative Medicine ,Vol.2019(2019)

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参考文献
[1] L. S. Yu, X. B. Li, Y. Y. Fan, G. H. Ye. et al.(2017). Expression of KGF-1 and KGF-2 in skin wounds and its application in forensic pathology. The American Journal of Forensic Medicine and Pathology.38(3):199-210. DOI: 10.1096/fj.201701506RR.
[2] X. Su, Y. Song, J. Jiang, C. Bai. et al.(2004). The role of aquaporin-1 (AQP1) expression in a murine model of lipopolysaccharide-induced acute lung injury. Respiratory Physiology & Neurobiology.142(1):1-11. DOI: 10.1096/fj.201701506RR.
[3] D. Impellizzeri, G. Bruschetta, E. Esposito, S. Cuzzocrea. et al.(2015). Emerging drugs for acute lung injury. Expert Opinion on Emerging Drugs.20(1):75-89. DOI: 10.1096/fj.201701506RR.
[4] X. Ma, H. Zhang, Q. Pan, Y. Zhao. et al.(2013). Hypoxia/aglycemia-induced endothelial barrier dysfunction and tight junction protein downregulation can be ameliorated by citicoline. PLoS ONE.8(12). DOI: 10.1096/fj.201701506RR.
[5] B. Chen, Z. Yang, C. Yang, W. Qin. et al.(2018). A self-organized actomyosin drives multiple intercellular junction disruption and directly promotes neutrophil recruitment in lipopolysaccharide-induced acute lung injury. The FASEB Journal.32(11):6197-6211. DOI: 10.1096/fj.201701506RR.
[6] J. Bi, L. Tong, X. Zhu, D. Yang. et al.(2014). Keratinocyte growth factor-2 intratracheal instillation significantly attenuates ventilator-induced lung injury in rats. Journal of Cellular and Molecular Medicine.18(6):1226-1235. DOI: 10.1096/fj.201701506RR.
[7] S. M. Armstrong, C. Wang, J. Tigdi, X. Si. et al.(2012). Influenza infects lung microvascular endothelium leading to microvascular leak: role of apoptosis and claudin-5. PLoS ONE.7(10). DOI: 10.1096/fj.201701506RR.
[8] H. L. Deissler, H. Deissler, G. K. Lang, G. E. Lang. et al.(2013). VEGF but not PlGF disturbs the barrier of retinal endothelial cells. Experimental Eye Research.115:162-171. DOI: 10.1096/fj.201701506RR.
[9] P. T. Filipczak, A. P. Senft, J. Seagrave, W. Weber. et al.(2015). NOS-2 inhibition in phosgene-induced acute lung injury. Toxicological Sciences.146(1):89-100. DOI: 10.1096/fj.201701506RR.
[10] B. Schlingmann, S. A. Molina, M. Koval. (2015). Claudins: gatekeepers of lung epithelial function. Seminars in Cell & Developmental Biology.42:47-57. DOI: 10.1096/fj.201701506RR.
[11] X. Fang, L. Wang, L. Shi, C. Chen. et al.(2014). Protective effects of keratinocyte growth factor-2 on ischemia–reperfusion–induced lung injury in rats. American Journal of Respiratory Cell and Molecular Biology.50(6):1156-1165. DOI: 10.1096/fj.201701506RR.
[12] K. Bäsler, S. Bergmann, M. Heisig, A. Naegel. et al.(2016). The role of tight junctions in skin barrier function and dermal absorption. Journal of Controlled Release.242:105-118. DOI: 10.1096/fj.201701506RR.
[13] S. Saksena, S. Priyamvada, A. Kumar, M. Akhtar. et al.(2013). Keratinocyte growth factor-2 stimulates P-glycoprotein expression and function in intestinal epithelial cells. American Journal of Physiology-Gastrointestinal and Liver Physiology.304(6):G615-G622. DOI: 10.1096/fj.201701506RR.
[14] J. Moitra, S. Sammani, J. G. Garcia. (2007). Re-evaluation of Evans Blue dye as a marker of albumin clearance in murine models of acute lung injury. Translational Research.150(4):253-265. DOI: 10.1096/fj.201701506RR.
[15] J. Wang, H. Chen, Y. Wang. (2016). Therapeutic efficacy of a mutant of keratinocyte growth factor-2 on trinitrobenzene sulfonic acid-induced rat model of Crohn's disease. American Journal of Translational Research.8:530-543. DOI: 10.1096/fj.201701506RR.
[16] S. Chen, S. Zheng, Z. Liu, C. Tang. et al.(2015). Endogeous sulfur dioxide protects against oleic acid-induced acute lung injury in association with inhibition of oxidative stress in rats. Laboratory Investigation.95(2):142-156. DOI: 10.1096/fj.201701506RR.
[17] C. M. Van Itallie, J. M. Anderson. (2014). Architecture of tight junctions and principles of molecular composition. Seminars in Cell & Developmental Biology.36:157-165. DOI: 10.1096/fj.201701506RR.
[18] T. J. Caron. (2015). Tight junction disruption: and dysregulation of the gastric mucosal barrier. World Journal of Gastroenterology.21(40). DOI: 10.1096/fj.201701506RR.
[19] M. Zhou, K. Osanai, M. Kobayashi, T. Oikawa. et al.(2014). Adenovector-mediated gene transfer of lysophosphatidylcholine acyltransferase 1 attenuates oleic acid–induced acute lung injury in rats. Critical Care Medicine.42(11):e716-e724. DOI: 10.1096/fj.201701506RR.
[20] L. Tong, J. Bi, X. Zhu. (2014). Keratinocyte growth factor-2 is protective in lipopolysaccharide-induced acute lung injury in rats. Respiratory Physiology & Neurobiology.201:7-14. DOI: 10.1096/fj.201701506RR.
[21] X. Shi, H. Liu, S. Li, H. Xu. et al.(2018). Keratinocyte growth factor protects endometrial cells from oxygen glucose deprivation/re-oxygenation via activating Nrf2 signaling. Biochemical and Biophysical Research Communications.501(1):178-185. DOI: 10.1096/fj.201701506RR.
[22] Y.-Y. Kim, S. Lee, M.-J. Kim, B.-C. Kang. et al.(2017). Tyrosol attenuates lipopolysaccharide-induced acute lung injury by inhibiting the inflammatory response and maintaining the alveolar capillary barrier. Food and Chemical Toxicology.109:526-533. DOI: 10.1096/fj.201701506RR.
[23] S. Herold, N. M. Gabrielli, I. Vadász. (2013). Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction. American Journal of Physiology-Lung Cellular and Molecular Physiology.305(10):L665-L681. DOI: 10.1096/fj.201701506RR.
[24] H. I. Chen, N. Hsieh, S. J. Kao, C. Su. et al.(2008). Protective effects of propofol on acute lung injury induced by oleic acid in conscious rats. Critical Care Medicine.36(4):1214-1221. DOI: 10.1096/fj.201701506RR.
[25] J. Bhattacharya, M. A. Matthay. (2013). Regulation and repair of the alveolar-capillary barrier in acute lung injury. Annual Review of Physiology.75:593-615. DOI: 10.1096/fj.201701506RR.
[26] D. Vestweber, M. Winderlich, G. Cagna, A. F. Nottebaum. et al.(2009). Cell adhesion dynamics at endothelial junctions: VE-cadherin as a major player. Trends in Cell Biology.19(1):8-15. DOI: 10.1096/fj.201701506RR.
[27] M. Koval. (2013). Claudin heterogeneity and control of lung tight junctions. Annual Review of Physiology.75:551-567. DOI: 10.1096/fj.201701506RR.
[28] S. E. Gill, M. Rohan, S. Mehta. (2015). Role of pulmonary microvascular endothelial cell apoptosis in murine sepsis-induced lung injury in vivo. Respiratory Research.16(1, article 109):1-13. DOI: 10.1096/fj.201701506RR.
[29] M. Giannotta, M. Trani, E. Dejana. (2013). VE-cadherin and endothelial adherens junctions: active guardians of vascular integrity. Developmental Cell.26(5):441-454. DOI: 10.1096/fj.201701506RR.
[30] P. Shao, J. Zhu, H. Ding. (2018). Tripterygium hypoglaucum (Levl.) Hutch attenuates oleic acid-induced acute lung injury in rats through up-regulating claudin-5 and ZO-1 expression. International Journal of Clinical and Experimental Medicine.11:6634-6647. DOI: 10.1096/fj.201701506RR.
[31] N. Feng, Q. Wang, J. Zhou, J. Li. et al.(2016). Keratinocyte growth factor-2 inhibits bacterial infection with Pseudomonas aeruginosa pneumonia in a mouse model. Journal of Infection and Chemotherapy.22(1):44-52. DOI: 10.1096/fj.201701506RR.
[32] A. Lerner, T. Matthias. (2015). Changes in intestinal tight junction permeability associated with industrial food additives explain the rising incidence of autoimmune disease. Autoimmunity Reviews.14(6):479-489. DOI: 10.1096/fj.201701506RR.
[33] J. Cai, G. Dou, L. Zheng, T. Yang. et al.(2015). Pharmacokinetics of topically applied recombinant human keratinocyte growth factor-2 in alkali-burned and intact rabbit eye. Experimental Eye Research.136:93-99. DOI: 10.1096/fj.201701506RR.
[34] R. Sweeney, M. Griffiths, D. McAuley. (2013). Treatment of acute lung injury: current and emerging pharmacological therapies. Seminars in Respiratory and Critical Care Medicine.34(04):487-498. DOI: 10.1096/fj.201701506RR.
[35] S. M. Krug, J. D. Schulzke, M. Fromm. (2014). Tight junction, selective permeability, and related diseases. Seminars in Cell & Developmental Biology.36:166-176. DOI: 10.1096/fj.201701506RR.
[36] H. C. Müller-Redetzky, W. Kummer, U. Pfeil, K. Hellwig. et al.(2012). Intermedin stabilized endothelial barrier function and attenuated ventilator-induced lung injury in mice. PLoS ONE.7(5). DOI: 10.1096/fj.201701506RR.
[37] L. B. Ware, M. A. Matthay. (2002). Keratinocyte and hepatocyte growth factors in the lung: Roles in lung development, inflammation, and repair. American Journal of Physiology-Lung Cellular and Molecular Physiology.282(5):L924-L940. DOI: 10.1096/fj.201701506RR.
[38] Y. Yang, S. Hu, X. Xu. (2016). The vascular endothelial growth factors-expressing character of mesenchymal stem cells plays a positive role in treatment of acute lung injury. Mediators of Inflammation.2016-12. DOI: 10.1096/fj.201701506RR.
[39] C. Gu, M. Liu, T. Zhao, D. Wang. et al.(2015). Protective role of p120-catenin in maintaining the integrity of adherens and tight junctions in ventilator-induced lung injury. Respiratory Research.16(1):1-15. DOI: 10.1096/fj.201701506RR.
[40] J. She, A. Goolaerts, J. Shen, J. Bi. et al.(2012). KGF-2 targets alveolar epithelia and capillary endothelia to reduce high altitude pulmonary oedema in rats. Journal of Cellular and Molecular Medicine.16(12):3074-3084. DOI: 10.1096/fj.201701506RR.
[41] K. G. Davidson, A. D. Bersten, H. A. Barr, K. D. Dowling. et al.(2000). Lung function, permeability, and surfactant composition in oleic acid-induced acute lung injury in rats. American Journal of Physiology-Lung Cellular and Molecular Physiology.279(6):L1091-L1102. DOI: 10.1096/fj.201701506RR.
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