Trimetazidine increases cell survival and inhibits the activation of inflammatory response in sodium taurocholate–induced acute pancreatitis
International Surgery, cilt.102, sa.11-12, ss.542-551, 2017 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 102 Sayı: 11-12
- Basım Tarihi: 2017
- Doi Numarası: 10.9738/intsurg-d-17-00122.1
- Dergi Adı: International Surgery
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.542-551
- Anahtar Kelimeler: Acute pancreatitis, Mitochondria, Trimetazidine, Mast cell, Oxidative stress, Experimental
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- Lokman Hekim Üniversitesi Adresli: Hayır
Özet
© 2017 Isik et al.Objective: To evaluate the therapeutic effects of trimetazidine (TMZ) in an experimental acute pancreatitis (AP) model induced with sodium taurocholate (STC). Summary of Background Data: At present, AP is considered a disease with no specific treatment. Preventing mitochondrial dysfunction in acinar cells may be an option for specific treatment of AP. TMZ is an anti-ischemic drug with anti-inflammatory, antioxidant, and mitochondrial modulatory effects. Methods: Rats were divided into 4 groups. AP was induced in the AP (n ¼ 7) and AP þ TMZ (n ¼ 7) groups by an injection of 4% sodium taurocholate to the pancreatic duct. The sham (n ¼ 6) and drug (n ¼ 6) groups were designated as control groups. The AP þ TMZ and drug groups were administered TMZ. Samples were taken at 72 hours, and histopathologic changes as well as biochemical parameters were analyzed. Results: Serum amylase, tissue myeloperoxidase activity, malondialdehyde levels, serum cytokine levels, and mast cell degranulation rates were elevated after induction of AP, whereas tissue antioxidant enzyme activities and cell viability rates [determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay] decreased. These parameters were found to be different in the AP group compared with those in all other groups (P, 0.05). A significant improvement of all parameters was achieved with the TMZ treatment of AP. Histologically, significant differences were found between the AP and AP þ TMZ groups in terms of leukocyte infiltration, necrosis, and apoptotic cell counts. Conclusions: In this study, we demonstrated that TMZ treatment protected the mitochondrial function and prevented the activation of the inflammatory cascade in the sodium taurocholate–induced AP model.