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Dergiler / European Journal of Biology / 2019 / Cilt: 78 - Sayı: 2

Effects of Tempol in Lipopolysaccharide-Induced Liver Injury

Tuğba KASKAVALCI
Huri BULUT
Cihan Demirci TANSEL
Perihan SİNEM SERİN
Erman Caner BULUT
Aslı KANDİL
Sayfa
144–152
Yayın Tarihi
2022-10-12
DOI
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⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

Theseresults may contribute to a better understanding of the role of tempol and basic mechanisms of underlying oxidative stressrelatedliver injury for further investigations.

📌 3 Maddede Bu Makale

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Amaç & Hipotez:Objective: Sepsis leads to conditions such as inflammatory and anti-inflammatory process, circulatory abnormalities, cellularand humoral reactions.
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Temel Bulgular & Veri:The aim of this study was to evaluate theeffects of a radical scavenger Tempol in lipopolysaccharide (LPS)-induced liver injury in rats.Materials and Methods: Male Wistar rats were divided into four groups: Control, LPS (15 mg/kg), LPS + Tempol group (100mg/kg Tempol, three hours after LPS administration) and Tempol (100 mg/kg).
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Sonuç & Katkı:Theseresults may contribute to a better understanding of the role of tempol and basic mechanisms of underlying oxidative stressrelatedliver injury for further investigations.
🔬Tür:Araştırma Makalesi
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Alan Parametreleri

Abstract

Objective: Sepsis leads to conditions such as inflammatory and anti-inflammatory process, circulatory abnormalities, cellularand humoral reactions. Endotoxin-induced oxidative stress causes injury in the liver. The aim of this study was to evaluate theeffects of a radical scavenger Tempol in lipopolysaccharide (LPS)-induced liver injury in rats.Materials and Methods: Male Wistar rats were divided into four groups: Control, LPS (15 mg/kg), LPS + Tempol group (100mg/kg Tempol, three hours after LPS administration) and Tempol (100 mg/kg). Blood glucose and body temperature weremeasured during the experiment. Superoxide dismutase (SOD), aspartate aminotransferase (AST), alanine aminotransferase(ALT) and C-reactive protein (CRP) levels were measured in plasma or liver tissue. Furthermore, histopathological changes andmyeloperoxidase-stained leukocytes infiltration were assessed in liver tissue.Results: LPS caused tissue damage and leukocytes infiltration, increased AST, ALT and CRP levels, and decreased bodytemperature, blood glucose and SOD levels. Tempol reduced AST and ALT levels and increased SOD levels. Tempol did notprevent tissue damage, leukocytes infiltration and increment of CRP levels. There were no changes in body temperature andblood glucose levels.Conclusion: The present study suggests that tempol may have antioxidant properties in LPS-induced liver injury. Theseresults may contribute to a better understanding of the role of tempol and basic mechanisms of underlying oxidative stressrelatedliver injury for further investigations.

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Bu Makaleye Atıf Yap

KASKAVALCI, T., BULUT, H., TANSEL, C. D., SERİN, P. S., BULUT, E. C., KANDİL, A. (2022). Effects of Tempol in Lipopolysaccharide-Induced Liver Injury. European Journal of Biology, Cilt: 78 - Sayı: 2, 144–152. https://ajindex.com/articles/510597

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Kaynakça (16)

  1. Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Intensive Care Med 2003; 29(4): 530-8
  2. Annane D, Bellissant E, Cavaillon JM. Septic shock. Lancet 2005; 365(9453): 63-78
  3. Minasyan H. Sepsis and septic shock: Pathogenesis and treatment perspectives. J Crit Care 2017; 40: 229-42
  4. Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med 2013; 369(9): 840-51
  5. Nesseler N, Launey Y, Aninat C, Morel F, Mallédant Y, Seguin P. Clinical review: The liver in sepsis. Crit Care 2012; 16(5):235
  6. Woźnica EA, Inglot M, Woźnica RK, Łysenko L. Liver dysfunction in sepsis. Adv Clin Exp Med 2018; 27(4): 547-51
  7. Koch A, Horn A, Dückers H, Yagmur E, Sanson E, Bruensing J, et al. Increased liver stiffness denotes hepatic dysfunction and mortality risk in critically ill non-cirrhotic patients at a medical ICU. Crit Care 2011; 15(6): 266
  8. Recknagel P, Gonnert FA, Westermann M, Lambeck S, Lupp A, Rudiger A, et al. Liver dysfunction and phosphatidylinositol-3- kinase signalling in early sepsis: experimental studies in rodent models of peritonitis. PLoS Med 2012; 9(11): e1001338
  9. Wang P, Ayala A, Ba ZF, Zhou M, Perrin MM, Chaudry IH. Tumor necrosis factor-alpha produces hepatocellular dysfunction despite normal cardiac output and hepatic microcirculation. Am J Physiol1993; 265(1 Pt 1): G126-32
  10. Dhainaut JF, Marin N, Mignon A, Vinsonneau C. Hepatic response to sepsis: interaction between coagulation and inflammatory processes. Crit Care Med 2001; 29(7 Suppl): 42-7
  11. Garofalo AM, Lorente-Ros M, Goncalvez G, Carriedo D, Ballén- Barragán A, Villar-Fernández A, et al. Histopathological changes of organ dysfunction in sepsis. Intensive Care Med Exp 2019; 7(Suppl 1):45
  12. Mannaa, FA, Abdel-Wahhab, KG. Physiological potential of cytokines and liver damages. Hepatoma Res 2016; 2: 131-43
  13. Szabo G, Romics L Jr, Frendl G. Liver in sepsis and systemic inflammatory response syndrome. Clin Liver Dis 2002; 6(4): 1045- 66
  14. Strnad P, Tacke F, Koch A, Trautwein C. Liver - guardian, modifier and target of sepsis. Nat Rev Gastroenterol Hepatol 2017; 14(1): 55-66
  15. Ring A, Stremmel W. The hepatic microvascular responses to sepsis. Semin Thromb Hemost 2000; 26(5): 589-94
  16. Wong CH, Jenne CN, Petri B, Chrobok NL, Kubes P. Nucleation of platelets with blood-borne pathogens on Kupffer cells precedes other innate immunity and contributes to bacterial clearan