title: Nadroparin sodium activates Nrf2/HO-1 pathway in acetic acid-induced colitis in rats.
abstract: Effects of nadroparin sodium, a low molecular weight heparin, in colitis was investigated by analyzing proteins implicated in nuclear factor E2-related factor-2/heme oxygenase-1 (Nrf2/HO-1) and nuclear factor kappa B (NF-κB) pathways. Twenty-eight rats were used. Colitis was induced by acetic acid (AA). Nadroparin sodium was given to prevention and treatment groups in addition to AA. Colitis was assessed histologically and levels of proteins were analyzed with Western blot. Nadroparin not only prevented and ameliorated the AA-induced colitis histopathologically but also decreased expression of colon NF-κB, activator protein-1, cyclooxygenase-2, tumor necrosis factor-alpha, and IL-6, which were significantly increased in group AA compared to control. The accumulation of Nrf2 in nuclear fraction and HO-1 found low in group AA was increased with nadroparin (p < 0.05). The mean malondialdehyde level increased with AA and was decreased significantly with nadroparin prevention and treatment (p < 0.001). Nadroparin sodium has both protective and therapeutic effects against colonic inflammation via exerting anti-oxidative and anti-inflammatory effects by modulating Nrf2/HO-1 and NF-κB pathways.
authors.affiliation: Department of Gastroenterology, School of Medicine, Firat University, 23200 Elazig, Turkey. mehmetyalniz@hotmail.com
authors.forename: Mehmet
authors.initials: M
authors.lastname: Yalniz
authors.forename: Ulvi
authors.initials: U
authors.lastname: Demirel
authors.forename: Cemal
authors.initials: C
authors.lastname: Orhan
authors.forename: Ibrahim Halil
authors.initials: IH
authors.lastname: Bahcecioglu
authors.forename: Ibrahim Hanefi
authors.initials: IH
authors.lastname: Ozercan
authors.forename: Cem
authors.initials: C
authors.lastname: Aygun
authors.forename: Mehmet
authors.initials: M
authors.lastname: Tuzcu
authors.forename: Kazim
authors.initials: K
authors.lastname: Sahin
mesh_terms: D019342:Acetic Acid; D000818:Animals; D003092:Colitis / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D003106:Colon / Q000187:drug effects / Q000473:pathology; D051546:Cyclooxygenase 2 / Q000096:biosynthesis; D051547:Heme Oxygenase-1 / Q000378:metabolism*; D015212:Inflammatory Bowel Diseases / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D015850:Interleukin-6 / Q000096:biosynthesis; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D051267:NF-E2-Related Factor 2 / Q000187:drug effects / Q000378:metabolism*; D016328:NF-kappa B / Q000378:metabolism*; D017762:Nadroparin / Q000494:pharmacology* / Q000627:therapeutic use; D018384:Oxidative Stress / Q000187:drug effects; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D018808:Transcription Factor AP-1 / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D015850:Interleukin-6; D051267:NF-E2-Related Factor 2; D016328:NF-kappa B; D017762:Nadroparin; C495637:Nfe2l2 protein, rat; D017382:Reactive Oxygen Species; D018808:Transcription Factor AP-1; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D051547:Heme Oxygenase-1; D051546:Cyclooxygenase 2; D019342:Acetic Acid