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Czasopismo

2015 | 74 | 3 |

Tytuł artykułu

Curcumin ameliorates experimental autoimmune acute myocarditis in rats as evidenced by decrease in thioredoxin immunoreactivity

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
This study was performed to investigate the effect of curcumin on cardiac myosin- -induced autoimmune myocarditis in rats and the change in thioredoxin (TRX) immunoreactivity in cardiomyocytes following curcumin treatment. Twenty-four six-week-old male Wistar rats were randomly allocated into 4 groups of 6 rats each. Group I received neither curcumin nor myosin. Group II received an oral solution of 1 g/kg/day of curcumin daily, from day 1 to day 21. To induce myocarditis, animals of both group III and group IV were injected by 1 mg of porcine cardiac myosin on days 1 and 8. In addition, animals of group IV received an oral solution of 1 g/kg/day of curcumin daily, from day 1 to day 21. Serum levels of creatine phosphokinase, troponin-T, tumour necrosis factor-alpha and interleukin-6 were estimated. Hearts were processed for histopathological and immunohistochemical studies. Serum biomarkers levels were significantly increased in myocarditis group as compared to other groups. The intake of curcumin significantly reduced the deviation in these markers. Sections of the wall of the heart from myocarditis group were characterised by inflammatory cell infiltration. Most of cardiomyocytes showed pyknotic nuclei and increased sarcoplasmic eosinophilia with strong immunoreactivity for TRX. Sections from myocarditis-curcumin group showed normal architecture with moderate immunoreactivity for TRX. The present study demonstrated that curcumin ameliorates acute myocarditis in rats and encouraged the estimation of serum level of TRX as a relevant indicator for the evaluation of the progress of acute myocarditis. (Folia Morphol 2015; 74, 3: 318–324)

Słowa kluczowe

Wydawca

-

Czasopismo

Rocznik

Tom

74

Numer

3

Opis fizyczny

p.318-324,fig.,ref.

Twórcy

autor
  • Department of Anatomy, College of Medicine, King Saud University, Riyadh, Saudi Arabia
  • Department of Anatomy, College of Medicine, King Saud University, Riyadh, Saudi Arabia
autor
  • Department of Anatomy, College of Medicine, King Saud University, Riyadh, Saudi Arabia
  • Department of Histology, Faculty of Medicine, Cairo University, Cairo, Egypt
autor
  • Department of Anatomy, College of Medicine, King Saud University, Riyadh, Saudi Arabia
  • Department of Pharmacology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia
  • Department of Pharmacology, College of Pharmacy, Al-Azhar University, Cairo, Egypt
  • Stem Cell Unit, Department of Anatomy, College of Medicine, King Saud University, Riyadh, Saudi Arabia
  • Stem Cell Unit, Department of Anatomy, College of Medicine, King Saud University, Riyadh, Saudi Arabia

Bibliografia

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  • 2. Blauwet L, Cooper L (2010) Myocarditis. Prog Cardiovasc Dis, 52: 274–288.
  • 3. Futamatsu H, Suzuki J, Kosuge H, Yokosei O, Kamad M, Ito H (2003) Attenuation of experimental autoimmune myocarditis by blocking activated T cells through inducible costimulatory molecule pathway. Cardiovasc Res, 59: 95–104.
  • 4. Hatcher H, Planalp R, Cho J, Torti FM (2008) Curcumin: from ancient medicine to current clinical trials. Cell Mol Life Sci, 65: 1631–1652.
  • 5. Kaden J (2007) IL-6 determination in serum of kidney graft recipients by a new bedside test: its diagnostic relevance. Transplant Proc, 39: 511–513.
  • 6. Kohli K, Ali J, Ansari M J, Raheman Z (2005) Curcumin: A natural anti-inflammatory agent. Indian J Pharacol, 37: 141–147.
  • 7. Li Y, Heusr J, Kosanke S, Hemric M, Cunningham M W (2005): Protection against experimental autoimmune myocarditis is mediated by interleukin-10-producing T cells that are controlled by dendritic cells. Am J Pathol, 167: 5–15.
  • 8. Liu W, Nakamura H, Shioji K, Tanito M, Oka S, Ahsan MK, Son A, Ishii Y, Kishimoto C, Yodoi J (2004) Thioredoxin-1 ameliorates myosin-induced autoimmune myocarditis by suppressing chemokine expressions and leucocyte chemotaxis in mice. Circulation, 110: 1276–1283.
  • 9. Lowenstein C J (2004) Exogenous thioredoxin reduces inflammation in autoimmune myocarditis. Circulation, 110: 1178–1179.
  • 10. Matsui Y, Okamoto H, Jia N, Akino M, Uede T, Kitabatake A, Nishihira J (2004) Blockade of macrophage migration inhibitory factor ameliorates experimental autoimmune myocarditis. J Mol Cell Cardiol, 37: 557–566.
  • 11. Menon VP, Sudheer AR (2007) Anti-oxidant and anti-inflammatory properties of curcumin. Advances in Experimental Medicine and Biology, 595: 105–125.
  • 12. Otsuka K, Terasaki F, Ikemoto M, Fujita S, Tsukada B, Katashima T, Kanzaki Y, Sohmiya K, Kono T, Toko H, Fujita M, Kitaura Y (2009) Suppression of inflammation in rat autoimmune myocarditis by S100A8/A9 through modulation of the pro-inflammatory cytokine network. Eur J Heart Fail, 11: 229–237.
  • 13. Rosenstein E, Zucker M, Kramer N (2000) Giant cell myocarditis: most fatal of autoimmune disease. Semin Arthritis Rheum, 30: 1–16.
  • 14. Shioji K, Kishimoto C, Nakamura H (2000) Up-regulation of thioredoxin (TRX) expression in giant cell myocarditis in rats. FEBS Lett, 472: 109–113.
  • 15. Tao L Gao E, Coletti C, Wang Y, Christopher T, Lopez B, Koch W, Ma X (2006) Thioredoxin reduces post-ischemic myocardial apoptosis by reducing oxidative/nitrative stress. Br J Pharmacol, 149: 311–318.
  • 16. Turoczi T, Chang VW, Engelman RM, Maulik N, Ho Y, Das DK (2003) Thioredoxin redox signaling in the ischemic heart: an insight with transgenic mice overexpressing Trx1. J Mol Cell Cardiol, 35: 695–704.
  • 17. Wahlstrom B, Blennow G (1978) A study on the fate of curcumin in the rat. Acta Pharmacol Toxicol, 43: 86–92.
  • 18. Wongcharoen W, Jai-Aue S, Phrommintikul A, Nawarawong W, Woragidpoonpol S, Tepsuwan T, Sukonthasarn A, Apaijai N, Chattipakorn N (2012) Effects of curcuminoids on frequency of acute myocardial infarction after coronary artery bypass grafting. Am J Cardiol, 110: 40–44.
  • 19. Yeh CH, Chen TP, Wu YC, Lin YN, Jing Lin P (2005) Inhibition of NF-kappaB activation with curcumin attenuates plasma inflammatory cytokines surge and cardiomyocytic apoptosis following cardiac ischemia/reperfusion. J Surg Res, 125: 109–116.
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Typ dokumentu

Bibliografia

Identyfikatory

Identyfikator YADDA

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