title: Nesfatin-1 alleviates extrahepatic cholestatic damage of liver in rats.
abstract: Obstructive jaundice (OJ) can be defined as cessation of bile flow into the small intestine due to benign or malignant changes. Nesfatin-1, recently discovered anorexigenic peptide derived from nucleobindin-2 in hypothalamic nuclei, was shown to have anti-inflammatory and antiapoptotic effects. This study is aimed to investigate the therapeutic effects of nesfatin-1 on OJ in rats. Twenty-four adult male Wistar-Hannover rats were randomly assigned to three groups: sham (n = 8), control (n = 8), and nesfatin (n = 8). After bile duct ligation, the study groups were treated with saline or nesfatin-1, for 10 days. Afterward, blood and liver tissue samples were obtained for biochemical analyses, measurement of cytokines, determination of the oxidative DNA damage, DNA fragmentation, and histopathologic analyses. Alanine aminotransferase and gamma-glutamyl transferase levels were decreased after the nesfatin treatment; however, these drops were statistically non-significant compared to control group (p = 0.345, p = 0.114). Malondialdehyde levels decreased significantly in nesfatin group compared to control group (p = 0.032). Decreases in interleukin-6 and tumor necrosis factor-α levels from the liver tissue samples were not statistically significant in nesfatin group compared to control group. The level of oxidative DNA damage was lower in nesfatin group, however this result was not statistically significant (p = 0.75). DNA fragmentation results of all groups were similar. Histopathological examination revealed that there was less neutrophil infiltration, edema, bile duct proliferation, hepatocyte necrosis, basement membrane damage, and parenchymal necrosis in nesfatin compared to control group. The nesfatin-1 treatment could alleviate cholestatic liver damage caused by OJ due to its anti-inflammatory and antioxidant effects.
authors: General Surgery Clinic, Bağcılar Training and Research Hospital, Istanbul, Turkey. solmazali@hotmail.com.
authors: Ali
authors: A
authors: Solmaz
authors: Osman Bilgin
authors: OB
authors: Gülçiçek
authors: Candaş
authors: C
authors: Erçetin
authors: Hakan
authors: H
authors: Yiğitbaş
authors: Erkan
authors: E
authors: Yavuz
authors: Sinan
authors: S
authors: Arıcı
authors: Can
authors: C
authors: Erzik
authors: Oğuzhan
authors: O
authors: Zengi
authors: Pelin
authors: P
authors: Demirtürk
authors: Atilla
authors: A
authors: Çelik
authors: Fatih
authors: F
authors: Çelebi
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D002135:Calcium-Binding Proteins / Q000627:therapeutic use*; D002779:Cholestasis / Q000188:drug therapy* / Q000473:pathology; D016207:Cytokines / Q000097:blood / Q000378:metabolism; D004249:DNA Damage; D053938:DNA Fragmentation; D004268:DNA-Binding Proteins / Q000627:therapeutic use*; D008099:Liver / Q000473:pathology*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D009419:Nerve Tissue Proteins / Q000627:therapeutic use*; D020556:Neutrophil Infiltration; D000080866:Nucleobindins; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar
chemical_list: D002135:Calcium-Binding Proteins; D016207:Cytokines; D004268:DNA-Binding Proteins; D009419:Nerve Tissue Proteins; C000630652:Nucb1 protein, rat; D000080866:Nucleobindins; D008315:Malondialdehyde; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase