title: Curcumin protects against ischemia/reperfusion injury in rat skeletal muscle.
abstract: BACKGROUND
  Curcumin has been shown to decrease ischemia-reperfusion (I/R) injury in kidney or brain tissues. In this study, the effects of curcumin were evaluated in skeletal muscle during I/R injury.
  
  
  METHODS
  Hind limb ischemia was induced by clamping the common femoral artery and vein. After 4 h ischemia, the clamp of the femoral vessels of animals was taken off and the animal underwent 2 h reperfusion. We measured plasma concentrations of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) using enzyme-linked immunosorbent assay (ELISA). The right gastrocnemius muscle was harvested and immediately stored at -30°C for the assessment of superoxide dismutase (SOD), catalase (CAT) activities, and measurement of glutathione (GSH), malondialdehyde (MDA), and protein oxidation (PO) levels. Curcumin (100 mg/kg), α-tocopherol, and normal saline (10 mL /kg1) were administered intraperitoneally 1 h prior reperfusion.
  
  
  RESULTS
  Plasma TNF-α or IL-1β levels increased significantly in I/R group. The plasma levels of these proinflammatory cytokines were reduced in curcumin group. Muscle tissues of I/R groups revealed significantly higher antioxidant enzyme (superoxide dismutase, glutathione peroxidase, catalase) activities, and increased levels of malondialdehyde, nitric oxide, and protein carbonyl content compared with the SHAM group. Levels of these parameters in muscle revealed significant reductions in the I/R + curcumin group compared witho the I/R group. Curcumin has more potent antioxidant activity than vitamin E in the skeletal muscle I/R.
  
  
  CONCLUSIONS
  In this study, protective effects of curcumin against skeletal muscle ischemia-reperfusion injury have been revealed. We underscore the necessity of human studies with curcumin that would be hypothetically beneficial preventing skeletal muscle I/R injury.
authors.affiliation: Department of Plastic and Reconstructive Surgery, Faculty of Medicine, Education and Research Hospital, Canakkale, Turkey.
authors.forename: Gulden
authors.initials: G
authors.lastname: Avci
authors.forename: Huseyin
authors.initials: H
authors.lastname: Kadioglu
authors.forename: Ahmet O
authors.initials: AO
authors.lastname: Sehirli
authors.forename: Suleyman
authors.initials: S
authors.lastname: Bozkurt
authors.forename: Oguz
authors.initials: O
authors.lastname: Guclu
authors.forename: Emrah
authors.initials: E
authors.lastname: Arslan
authors.forename: Sedit K
authors.initials: SK
authors.lastname: Muratli
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D003474:Curcumin / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D053583:Interleukin-1beta / Q000097:blood; D008315:Malondialdehyde / Q000378:metabolism; D023421:Models, Animal; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000378:metabolism; D010446:Peptide Fragments / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow / Q000187:drug effects* / Q000502:physiology; D015427:Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000975:Antioxidants; D053583:Interleukin-1beta; D010446:Peptide Fragments; D014409:Tumor Necrosis Factor-alpha; C052994:interleukin-1beta (163-171); D008315:Malondialdehyde; D002374:Catalase; D013482:Superoxide Dismutase; D005978:Glutathione; D003474:Curcumin