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Effects of lexipafant (BB-882), a platelet activating factor receptor antagonist, on liver damage due to bile duct ligation in rats   
Yazarlar
Prof. Dr. Hülya ÖZTÜRK Prof. Dr. Hülya ÖZTÜRK
Kırşehir Ahi Evran Üniversitesi, Türkiye
Hayrettin Ozturk
Ali Ihsan Dokucu
Selcuk Otcu
Özet
Background and study aims : Extrahepatic cholestasis is one of the main factors causing liver fibrosis. In this study, we aimed to evaluate the effects of lexipafant (BB-882), a platelet activating factor receptor antagonist, on liver damage in rats with bile duct ligation.
Methods: A total of 30 male Sprague-Dawley rats weighing 160-190 g were used in this study. Group I (Sham-control, n = 10) rats were undergone laparotomy alone and bile duct was just dissected from the surrounding tissue. Group 2 rats (BDL/Untreated, n = 10) were subjected to bile duct ligation and no drug was applied. Group 3 rats (BDUBB-882, n = 10) received a daily dose of BB-882 intraperitoneally for 14 days after BDL. At the end of the two-week period, biochemical and histological evaluation was processed.
Results : The mean serum bilirubin and liver enzymes level significantly decreased, and Superoxide dismutase, catalase and glutathione peroxidase values were significantly increased in BDL/BB-882 group when compared to BDUUntreated group. The histopathological score was significantly less in the BDUBB-882 group compared to the BDL/Untreated rats. In the BDL/BB-882 group was observed less fibrosis and neutrophil infiltration.
Conclusions : These results suggest that BB-882 (lexipafant) may reduce the severity of the inflammatory response to liver injury produced by bile duct ligation in rats.
Anahtar Kelimeler
bile duct ligation | BB-882 | lexipafant | rat
Makale Türü Özgün Makale
Makale Alt Türü SSCI, AHCI, SCI, SCI-Exp dergilerinde yayımlanan tam makale
Dergi Adı ACTA GASTRO-ENTEROLOGICA BELGICA
Dergi ISSN 1784-3227
Dergi Grubu Q4
Makale Dili İngilizce
Basım Tarihi 04-2006
Cilt No 69
Sayı 2
Sayfalar 197 / 202
BM Sürdürülebilir Kalkınma Amaçları
Atıf Sayıları
WoS 2

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