Chitosan and blueberry treatment induces arginase activity and inhibits nitric oxide production during acetaminophen-induced hepatotoxicity

ÖZÇELİK E., USLU S., BURUKOĞLU DÖNMEZ D., MUSMUL A.

PHARMACOGNOSY MAGAZINE, cilt.10, sa.38, ss.217-224, 2014 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 10 Sayı: 38
  • Basım Tarihi: 2014
  • Doi Numarası: 10.4103/0973-1296.133234
  • Dergi Adı: PHARMACOGNOSY MAGAZINE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED)
  • Sayfa Sayıları: ss.217-224
  • Anahtar Kelimeler: Acetaminophen hepatotoxicity, arginase, blueberry, chitosan, ornithine, INDUCED LIVER-INJURY, REDUCED GLUTATHIONE, DAMAGE, ANTIOXIDANT, EXTRACT, SERUM, MICE
  • Eskişehir Osmangazi Üniversitesi Adresli: Evet

Özet

Background: Liver diseases have become a major problem of the worldwide. More than 50% of all cases of liver failure can be attributed to drugs. Among these, acetaminophen is the most common cause. Objective: The aim of this study was to investigate the the hepatoprotective effects of blueberry and chitosan on tissue arginase activity, ornithine and nitric oxide levels during the acetaminophen-induced hepatotoxicity. Materials and Methods: Acetaminophen (250 mg/kg body weight per day), blueberry (60 mg/kg body weight per day) and, chitosan (200 mg/kg body weight per day) were administered to the rats by oral gavage during the experimental period. Results: Blueberry and chitosan significantly decreased liver arginase activity and ornithine levelsand and increased nitric oxide levels. Glutathione levels were remarkably increased by chitosan and blueberry treatments. Conclusion: The results of the present study indicate that blueberry and chitosan effectively protected against the acetaminophen-induced hepatotoxicity. The hepatoprotective effect afforded by blueberry and chitosan can be attributed to its antioxidant and anti-inflammatory activities.