Trimetazidine increases cell survival and inhibits the activation of inflammatory response in sodium taurocholate–induced acute pancreatitis

Creative Commons License

Isik S., Sengül N., Töre F., Aydın C., Aslan A., Uçar G., ...More

International Surgery, vol.102, no.11-12, pp.542-551, 2017 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 102 Issue: 11-12
  • Publication Date: 2017
  • Doi Number: 10.9738/intsurg-d-17-00122.1
  • Journal Name: International Surgery
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.542-551
  • Keywords: Acute pancreatitis, Mitochondria, Trimetazidine, Mast cell, Oxidative stress, Experimental
  • Lokman Hekim University Affiliated: No


© 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.