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The carvacrol ameliorates acute pancreatitis-induced liver injury via antioxidant response
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  • 作者:Murat Bakır ; Fatime Geyikoglu ; Suat Colak ; Hasan Turkez…
  • 刊名:Cytotechnology
  • 出版年:2016
  • 出版时间:August 2016
  • 年:2016
  • 卷:68
  • 期:4
  • 页码:1131-1146
  • 全文大小:2,287 KB
  • 刊物类别:Chemistry and Materials Science
  • 刊物主题:Chemistry
    Biotechnology
    Biomedicine
    Biochemistry
  • 出版者:Springer Netherlands
  • ISSN:1573-0778
  • 卷排序:68
文摘
Acute pancreatitis (AP) may cause significant persistent multi-organ dysfunction. Carvacrol (CAR) possesses a variety of biological and pharmacological properties. The aim of the present study was to analyze the hepatic protection of CAR on AP induced by cerulein and to explore the underlying mechanism using in vivo studies. The rats were randomized into groups to receive (1) no therapy; (2) 50 µg/kg cerulein at 1-h intervals by four intraperitoneal injection (i.p.); (3) 50, 100 and 200 mg/kg CAR by one i.p.; and (4) cerulein + CAR after 2 h of cerulein injection. 12 h later, serum was provided to assess the blood AST, ALT and LDH values. Also, liver tissues were obtained for histological and biochemical measurements. Liver oxidative stress markers were evaluated by changes in the amount of lipid peroxides measured as MDA and changes in tissue antioxidant enzyme levels, SOD, CAT and GSH-Px. Histopathological examination was performed using scoring systems. Oxidative damage to DNA was quantitated in studied tissues of experimental animals by measuring the increase in 8-hydroxydeoxyguanosine (8-OHdG) formations. We found that the increasing doses of CAR decreased pancreatitis-induced MDA and 8-OH-dG levels. Moreover, the liver SOD, CAT and GSH-Px activities in the AP + CAR group were higher than that of the rats in the AP group. In the treatment groups, AST, ALT and LDH were reduced. Besides, necrosis, coagulation and inflammation in the liver were alleviated (p < 0.05). We suggest that CAR could be a safe and potent new drug candidate for treating AP through its antioxidative mechanism of action for the treatment of a wide range of disorders related to hepatic dysfunction.KeywordsExperimental acute pancreatitisLiver damageCarvacrolAntioxidant responseOxidative DNA damageHistopathology

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