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

Effects of Tempol in Lipopolysaccharide-Induced Liver Injury

Pages
147–155
Publication Date
2019-12-06
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

These results may contribute to a better understanding of the role of tempol and basic mechanisms of underlying oxidative stressrelated liver injury for further investigations.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Sepsis leads to conditions such as inflammatory and anti-inflammatory process, circulatory abnormalities, cellular and humoral reactions.
📊
Key Findings & Data:Materials and Methods: Male Wistar rats were divided into four groups: Control, LPS (15 mg/kg), LPS + Tempol group (100 mg/kg Tempol, three hours after LPS administration) and Tempol (100 mg/kg).
💡
Conclusion & Impact:These results may contribute to a better understanding of the role of tempol and basic mechanisms of underlying oxidative stressrelated liver injury for further investigations.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Lipopolysaccharide · Liver · Tempol

Abstract

Objective: Sepsis leads to conditions such as inflammatory and anti-inflammatory process, circulatory abnormalities, cellular and humoral reactions. Endotoxin-induced oxidative stress causes injury in the liver. The aim of this study was to evaluate the effects 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 (100 mg/kg Tempol, three hours after LPS administration) and Tempol (100 mg/kg). Blood glucose and body temperature were measured 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 and myeloperoxidase-stained leukocytes infiltration were assessed in liver tissue. Results: LPS caused tissue damage and leukocytes infiltration, increased AST, ALT and CRP levels, and decreased body temperature, blood glucose and SOD levels. Tempol reduced AST and ALT levels and increased SOD levels. Tempol did not prevent tissue damage, leukocytes infiltration and increment of CRP levels. There were no changes in body temperature and blood glucose levels. Conclusion: The present study suggests that tempol may have antioxidant properties in LPS-induced liver injury. These results may contribute to a better understanding of the role of tempol and basic mechanisms of underlying oxidative stressrelated liver injury for further investigations.

🔖

Cite This Article

SERİN, P. S., KANDİL, A., BULUT, H., KASKAVALCİ, T., BULUT, E. C., DEMİRCİ-TANSEL, C. (2019). Effects of Tempol in Lipopolysaccharide-Induced Liver Injury. European Journal of Biology, Cilt: 78 - Sayı: 2, 147–155. https://ajindex.com/articles/33190

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (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-3kinase 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, BallénBarragán 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): 104566
  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 clearance. Na