Dynamic Changes of TNF-α in Isolated Rat Heart at Different Time Points afer Myocardial Hypoxia/Reoxygenation_Chinese Journal of Clinical Thoracic and Cardiovascular Surgery

Authors：

HEJin-bo ^1,2 , CHENLing-long ³ , WANGXian-yu ¹ , LUOZi-yin ² , LIUYa-kun ⁴ , WANGYang ² ,  WANGWan-tie ²

1. Department of Anesthesiology, Taihe Hospital, Hubei University of Medicine, Shiyan 442000 Hubei, P. R. China;
2. Ischemia/Reperfusion Injury Research Institute, Wenzhou Medical University, Whenzhou 325035 Zhejiang, P. R. China;
3. Department of Emergency of Wenzhou People's Hospital, Whenzhou 325035 Zhejiang, P. R. China;
4. Teaching and Research Office of Pathophysiology of Anhui Medical University, Hefei 230000, P. R. China;

Corresponding author：

WANGWan-tie, Email: wwt@wmu.edu.cn

Keywords：

Tumor necrosis factor-α(TNF-α); Myocardium; Hypoxia/reoxygenation; Hemodynamics

DOI：

10.7507/1007-4848.20150285

Video：

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Objective To investigate the expression of tumor necrosis factor α(TNF-α ) in isolated rat heart at different time points after myocardial hypoxia/reoxygenation. Methods The isolated langendorff perfused rat heart model was established. Forty-eight SD rats were randomly divided into four groups: a sham group, hypoxia/reoxygenation groups including a H/R 0.5 h group, a 1 h group and a 2 h group. The heart rate(HR), the 1eft ventricular development pressure(LVDP), maximal rates of increase/decrease of the left ventricular pressure(±dp/dt_max) were continuously recorded. The concentrations of TNF-α and creatine kinase-MB(CK-MB) in myocardium, mRNA expression of TNF-α in myocardium were tested. Ultra structure of myocardium was observed under electron microscope. Results The levels of LVDP, ±dp/dt_max, and HR of hypoxia/reoxygenation group were significantly lower than those in the sham group(P<0.05).The levels of TNF-α and CK-MB and the expressions of TNF-α at mRNA level in the hypoxia/reoxygenation group were higher than those in the sham group(P<0.05).There were significant differences in the above parameters among the H/R 0.5 h group, the 1 h group, the 2 h group(P<0.05).The concentrations of TNF-α and CK-MB, the mRNA expression of TNF-α were higher in the I/R 2 h group than those in the other two groups. Conclusion The high expression of TNF-α in myocardium after myocardial hypoxia/reoxygenation in rats is related to the degree of myocardium damage and may lead to myocardial injury.

Citation： HEJin-bo, CHENLing-long, WANGXian-yu, LUOZi-yin, LIUYa-kun, WANGYang, WANGWan-tie. Dynamic Changes of TNF-α in Isolated Rat Heart at Different Time Points afer Myocardial Hypoxia/Reoxygenation. Chinese Journal of Clinical Thoracic and Cardiovascular Surgery, 2015, 22(12): 1147-1151. doi: 10.7507/1007-4848.20150285 Copy

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2.	Bainey KR, Armstrong PW. Clinical perspectives on reperfusion injury in acute myocardial infarction. Am Heart J, 2014, 167(5):637-645.
3.	Garciarena CD, Fantinelli JC, Caldiz CI, et al. Myocardial reperfusion injury:reactive oxygen species vs NHE-1 reactivation. Cell Physiol Biochem, 2011, 27(1):13-22.
4.	Ma HJ, Li Q, Ma HJ, et al. Chronic intermittent hypobaric hypoxia ameliorate ischemia/reperfusion-induced calcium overload in heart via Na/Ca Exchanger in developing Rats. Cell Physiol Biochem, 2014, 34(2):313-324.
5.	Xu T, Wu X, Chen Q, et al. The anti-apoptotic and cardioprotective effects of salvianolic acid A on rat cardiomyocytes following ischemia/reperfusion by DUSP-mediated regulation of the ERK1/2/JNK pathway. PloS One, 2014, 9(7):e102292.
6.	Carswell EA, Old LJ, Kassel RL, et al. An endotoxin-induced serum factor that causes necrosis of tumors. Proc Natl Acad Sci USA, 1975, 72(9):3666-3670.
7.	Çekiç C, Aslan F, Vatansever S, et al. Latent tuberculosis screening tests and active tuberculosis infection rates in Turkish inflammatory bowel disease patients under anti-tumor necrosis factor therapy. Ann Gastroenterol, 2015,28(2):241-246.
8.	Dinh W, Futh R, Nickl W, et al. Elevated plasma levels of TNF-alpha and interleukin-6 in patients with diastolic dysfunction and glucose metabolism disorders. Cardiovasc Diabetol, 2009, 8(2):58.
9.	Ridker PM, Luscher TF. Anti-inflammatory therapies for cardiovascular disease. Eur Heart J, 2014, 35(27):1782-1791.
10.	何金波, 包财盈, 叶玉柱, 等. 缺氧/复氧大鼠心肌中IL-1β浓度的动态变化及意义. 中国应用生理学杂志,2015, 1:27-30.
11.	Ao L, Zou N, Cleveland JC, et al. Myocardial TLR4 is a determinant of neutrophil infiltration after global myocardial ischemia:mediating KC and MCP-1 expression induced by extracellular HSC70. Am J Physiol Heart Circ Physiol, 2009, 297(1):H21-H28.
12.	高思海, 肖诗亮, 杨辰垣. 三甲氧苄嗪对大鼠离体心脏再灌注损伤的保护作用.中国胸心血管外科临床杂志, 2002, 9(3):192-194.
13.	Zhang C, Huang Y, Zhang Q-Z, et al. Effect of bushen gujin recipe on serum and synovia interleukin-1 and tumor necrosis factor-alpha of knee osteoarthritis model rabbits. Zhongguo Zhong Xi Yi Jie He Za Zhi, 2015, 35(3):355-358.
14.	Cheng JZ, Yu D, Zhang H, et al. Inhibitive effect of IL-24 gene on CD133(+) laryngeal cancer cells. Asian Pac J Trop Med, 2014, 7(11):867-872.
15.	Golia E, Limongelli G, Natale F, et al. Inflammation and cardiovascular disease:from pathogenesis to therapeutic target. Curr Atheroscler Rep, 2014, 16(9):435.
16.	Brown WV, Remaley AT, Ridker PM. JCL Roundtable:Is inflammation a future target in preventing arteriosclerotic cardiovascular disease. J Clin Lipidol, 2015, 9(2):119-128.
17.	Rodrigues FL, Fais RS, Tostes RC, et al. There is a link between erectile dysfunction and heart failure:It could be inflammation. Curr Drug Targets, 2015, 16(5):442-450.
18.	Bironaite D, Daunoravicius D, Bogomolovas J, et al. Molecular mechanisms behind progressing chronic inflammatory dilated cardiomyopathy. BMC Cardiovasc Disord, 2015, 15(1):26.
19.	Zwerina J, Redlich K, Polzer K, et al. TNF-induced structural joint damage is mediated by IL-1. Proc Natl Acad Sci USA, 2007, 104(28):11742-11747.
20.	Kang MW, Song HJ, Kang SK, et al. Nafamostat mesilate inhibits TNF-α-induced vascular endothelial cell dysfunction by inhibiting reactive oxygen species production. Korean J Physiol Pharmacol, 2015, 19(3):229-234.
21.	Hayslip J, Dressler EV, Weiss H, et al. Plasma TNF-α and soluble TNF receptor levels after doxorubicin with or without Co-administration of mesna——A randomized, cross-over clinical study. PloS One, 2015, 10(4):e0124988.
22.	Wangensteen KJ, Zhang S, Greenbaum LE, et al. A genetic screen reveals Foxa3 and TNFR1 as key regulators of liver repopulation. Genes Dev, 2015, 29(9):904-909.
23.	Cabal-Hierro L, Lazo PS. Signal transduction by tumor necrosis factor receptors. Cell signal, 2012, 24(6):1297-1305.
24.	Fragoso Lona JM, Sierra Martinez M, Vargas Alarcon G, et al. Tumor necrosis factor alfa in cardiovascular diseases:molecular biology and genetics. Gac Med Mex, 2013, 149(5):521-530.
25.	Levine B, Kalman J, Mayer L, et al. Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N Engl J Med, 1990, 323(4):236-241.
26.	Cugno M, Ingegnoli F, Gualtierotti R, et al. Potential effect of anti-tumour necrosis factor-alpha treatment on reducing the cardiovascular risk related to rheumatoid arthritis. Curr Vasc Pharmacol, 2010, 8(2):285-292.

1. Waters RE 2nd, Singh KP, Roe MT, et al. Rationale and strategies for implementing community-based transfer protocols for primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarction. J Am Coll Cardiology, 2004, 43(12):2153-2159.
2. Bainey KR, Armstrong PW. Clinical perspectives on reperfusion injury in acute myocardial infarction. Am Heart J, 2014, 167(5):637-645.
3. Garciarena CD, Fantinelli JC, Caldiz CI, et al. Myocardial reperfusion injury:reactive oxygen species vs NHE-1 reactivation. Cell Physiol Biochem, 2011, 27(1):13-22.
4. Ma HJ, Li Q, Ma HJ, et al. Chronic intermittent hypobaric hypoxia ameliorate ischemia/reperfusion-induced calcium overload in heart via Na/Ca Exchanger in developing Rats. Cell Physiol Biochem, 2014, 34(2):313-324.
5. Xu T, Wu X, Chen Q, et al. The anti-apoptotic and cardioprotective effects of salvianolic acid A on rat cardiomyocytes following ischemia/reperfusion by DUSP-mediated regulation of the ERK1/2/JNK pathway. PloS One, 2014, 9(7):e102292.
6. Carswell EA, Old LJ, Kassel RL, et al. An endotoxin-induced serum factor that causes necrosis of tumors. Proc Natl Acad Sci USA, 1975, 72(9):3666-3670.
7. Çekiç C, Aslan F, Vatansever S, et al. Latent tuberculosis screening tests and active tuberculosis infection rates in Turkish inflammatory bowel disease patients under anti-tumor necrosis factor therapy. Ann Gastroenterol, 2015,28(2):241-246.
8. Dinh W, Futh R, Nickl W, et al. Elevated plasma levels of TNF-alpha and interleukin-6 in patients with diastolic dysfunction and glucose metabolism disorders. Cardiovasc Diabetol, 2009, 8(2):58.
9. Ridker PM, Luscher TF. Anti-inflammatory therapies for cardiovascular disease. Eur Heart J, 2014, 35(27):1782-1791.
10. 何金波, 包财盈, 叶玉柱, 等. 缺氧/复氧大鼠心肌中IL-1β浓度的动态变化及意义. 中国应用生理学杂志,2015, 1:27-30.
11. Ao L, Zou N, Cleveland JC, et al. Myocardial TLR4 is a determinant of neutrophil infiltration after global myocardial ischemia:mediating KC and MCP-1 expression induced by extracellular HSC70. Am J Physiol Heart Circ Physiol, 2009, 297(1):H21-H28.
12. 高思海, 肖诗亮, 杨辰垣. 三甲氧苄嗪对大鼠离体心脏再灌注损伤的保护作用.中国胸心血管外科临床杂志, 2002, 9(3):192-194.
13. Zhang C, Huang Y, Zhang Q-Z, et al. Effect of bushen gujin recipe on serum and synovia interleukin-1 and tumor necrosis factor-alpha of knee osteoarthritis model rabbits. Zhongguo Zhong Xi Yi Jie He Za Zhi, 2015, 35(3):355-358.
14. Cheng JZ, Yu D, Zhang H, et al. Inhibitive effect of IL-24 gene on CD133(+) laryngeal cancer cells. Asian Pac J Trop Med, 2014, 7(11):867-872.
15. Golia E, Limongelli G, Natale F, et al. Inflammation and cardiovascular disease:from pathogenesis to therapeutic target. Curr Atheroscler Rep, 2014, 16(9):435.
16. Brown WV, Remaley AT, Ridker PM. JCL Roundtable:Is inflammation a future target in preventing arteriosclerotic cardiovascular disease. J Clin Lipidol, 2015, 9(2):119-128.
17. Rodrigues FL, Fais RS, Tostes RC, et al. There is a link between erectile dysfunction and heart failure:It could be inflammation. Curr Drug Targets, 2015, 16(5):442-450.
18. Bironaite D, Daunoravicius D, Bogomolovas J, et al. Molecular mechanisms behind progressing chronic inflammatory dilated cardiomyopathy. BMC Cardiovasc Disord, 2015, 15(1):26.
19. Zwerina J, Redlich K, Polzer K, et al. TNF-induced structural joint damage is mediated by IL-1. Proc Natl Acad Sci USA, 2007, 104(28):11742-11747.
20. Kang MW, Song HJ, Kang SK, et al. Nafamostat mesilate inhibits TNF-α-induced vascular endothelial cell dysfunction by inhibiting reactive oxygen species production. Korean J Physiol Pharmacol, 2015, 19(3):229-234.
21. Hayslip J, Dressler EV, Weiss H, et al. Plasma TNF-α and soluble TNF receptor levels after doxorubicin with or without Co-administration of mesna——A randomized, cross-over clinical study. PloS One, 2015, 10(4):e0124988.
22. Wangensteen KJ, Zhang S, Greenbaum LE, et al. A genetic screen reveals Foxa3 and TNFR1 as key regulators of liver repopulation. Genes Dev, 2015, 29(9):904-909.
23. Cabal-Hierro L, Lazo PS. Signal transduction by tumor necrosis factor receptors. Cell signal, 2012, 24(6):1297-1305.
24. Fragoso Lona JM, Sierra Martinez M, Vargas Alarcon G, et al. Tumor necrosis factor alfa in cardiovascular diseases:molecular biology and genetics. Gac Med Mex, 2013, 149(5):521-530.
25. Levine B, Kalman J, Mayer L, et al. Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N Engl J Med, 1990, 323(4):236-241.
26. Cugno M, Ingegnoli F, Gualtierotti R, et al. Potential effect of anti-tumour necrosis factor-alpha treatment on reducing the cardiovascular risk related to rheumatoid arthritis. Curr Vasc Pharmacol, 2010, 8(2):285-292.

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