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H2 therapy protects myocardial cell injury induce by sepsis via attenuated expression the level of HMGB1

 
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Pathophysiology of Cell Injury Journal  Volume 1, Issue 1, pages 10-19 December 2012

Amy A Bravo; Krneta Kumm; Catalina Lamy; Jorge Jeanneau; Gisèle Cuello; Jack Lefer

Abstract

Sepsis involves a robust inflammatory response, involving up-regulated chemokine expression and leukocyte accumulation, contributes to the mechanism of myocardial injury and cardiac dysfunction. Currently, it is unknown whether H2 suppresses myocardial inflammatory response to sepsis. We tested the hypothesis that treated mouse by H2 protects the heart against sepsis and LV dysfunction through suppression of the high-mobility group box 1 protein (HMGB1) expression. Cecal ligation and puncture (CLP) was used to induce sepsis. By inhaled mice with 2% H2 for 1 h followed CLP in both sham and sepsis model mice was associated with reduced myocardial cell injury mainly associated with reduced expression of HMGB1. Furthermore, H2 treated animals associated with decreased numbers of monocyte and improved LV function. These findings suggest that this novel H2 has a therapeutic potential for the regulation of myocardial inflammatory response to sepsis.

Keywords: Sepsis; Hydrogen; Inflammatory response; HMGB1; CLP

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References

1. Martin GS, Mannino DM, Eaton S, Moss M. The epidemiology of sepsis in the United States from 1979 through 2000. The New England Journal of Medicine 2003;348(16):1546–1554. [PubMed]

2. Okazaki Y, Matsukawa A. Pathophysiology of sepsis and recent patents on the diagnosis, treatment and prophylaxis for sepsis. Recent Patents on Inflammation and Allergy Drug Discovery 2009;3(1):26–32. [PubMed]

3. Macallan DC, Griffin GE. Cardiac muscle protein gene expression in the endotoxin-treated rat. Clin Sci (Colch) 1994; 87:539–546. [PubMed]

4. Kumar A, Haery C, Parrillo JE. Myocardial dysfunction in septic shock. Crit Care Clin 2000;16:251-287. [PubMed]

5. Eichacker PQ, Natanson C, Danner RL. Surviving sepsis—practice guidelines, marketing campaigns, and Eli Lilly. The New England Journal of Medicine 2006;355(16):1640–1642. [PubMed]

6. Abraham E, Laterre P-F, Garg R, et al. Drotrecogin alfa (activated) for adults with severe sepsis and a low risk of death. The New England Journal of Medicine 2005;353(13):1332–1341. [PubMed]

7. Wang H, Li W, Goldstein R, Tracey KJ, Sama AE. HMGB1 as a potential therapeutic target. Novartis Found Symp 2007;280:73-85. [PubMed]

8. Yang H, Wang H, Czura CJ, Tracey KJ. HMGB1 as a cytokine and therapeutic target. J Endotoxin Res 2002;8(6):469-72. [PubMed]

9. Wang H, Yang H, Tracey KJ. Extracellular role of HMGB1 in inflammation and sepsis. J Intern Med 2004;255(3):320-31. [PubMed]

10. Andersson U, Erlandsson-Harris H, Yang H, Tracey KJ. HMGB1 as a DNA-binding cytokine. J Leukoc Biol 2002;72(6):1084-91.

11. Xie K, Yu Y, Zhang Z, et al. Hydrogen gas improves survival rate and organ damage in zymosan-induced generalized inflammation model. Shock 2010;34(5):495–501. [PubMed]

12. Ohsawa I, Ishikawa M, Takahashi K, et al. Hydrogen acts as a therapeutic antioxidant by selectively reducing cytotoxic oxygen radicals. Nature Medicine 2007;13(6):688–694. [PubMed]

13. Xie K, Yu Y, Pei Y, et al. Protective effects of hydrogen gas on murine polymicrobial sepsis via reducing oxidative stress and HMGB1 release. Shock 2010;34(1):90–97. [PubMed]

14. Toscano MG, Ganea D, Gamero AM. Cecal Ligation Puncture Procedure. J Vis Exp 2011; 51:2860. [Abstract/Full-Text]

15. Georgakopoulos D, Mitzner WA, Chen CH. In vivo murine left ventricular pressure-volume relations by miniaturized conductance micromanometry. Am J Physiol 1998;274(4 Pt 2):H1416-22. [PubMed]

16. Kim JY, Park JS, Strassheim D. HMGB1 contributes to the development of acute lung injury after hemorrhage. Am J Physiol Lung Cell Mol Physiol 2005;288(5):L958-65. [PubMed]

17. Silva E, Arcaroli J, He Q, et al. HMGB1 and LPS induce distinct patterns of gene expression and activation in neutrophils from patients with sepsis-induced acute lung injury. Intensive Care Med 2007; 33(10):1829-39. [PubMed]

18. Xing L, Remick DG. Relative cytokine and cytokine inhibitor production by mononuclear cells and neutrophils. Shock 2003; 20:10-16. [PubMed]

19. Tavener SA, Kubes P. Is there a role for cardiomyocyte toll-like receptor 4 in endotoxemia? Trends Cardiovasc Med 2005; 15:153-157. [PubMed]

20. Laird MD, Shields JS, Sukumari-Ramesh S, et al. High mobility group box protein-1 promotes cerebral edema after traumatic brain injury via activation of toll-like receptor 4. Glia 2014;62(1):26–38. [PubMed]

21. Yang H, Tracey KJ. Targeting HMGB1 in inflammation. Biochimica et Biophysica Acta 2010;1799(1-2):149–156. [PubMed]

22. Huang W, Tang Y, Li L. HMGB1, a potent proinflammatory cytokine in sepsis. Cytokine 2010;51(2):119–126. [PubMed]

23. Ohta S. Hydrogen gas and hydrogen water act as a therapeutic and preventive antioxidant with a novel concept. Nihon Ronen Igakkai Zasshi 2008;45(4):355–362. [PubMed]

24. Ohsawa I, Ishikawa M, Takahashi K, et al. Hydrogen acts as a therapeutic antioxidant by selectively reducing cytotoxic oxygen radicals. Nature Medicine 2007;13(6):688–694. [PubMed]

 

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