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RETRACTED: Melatonin inhibits the expression of the inducible isoform of nitric oxide synthase and nuclear factor kappa B activation in rat skeletal muscle
Author(s) -
Alonso María,
Collado Pilar S.,
GonzálezGallego Javier
Publication year - 2006
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1111/j.1600-079x.2006.00323.x
Subject(s) - melatonin , endocrinology , medicine , nitric oxide synthase , nitric oxide , oxidative stress , glutathione , skeletal muscle , chemistry , nf κb , iκb kinase , signal transduction , biology , inflammation , biochemistry , enzyme
This study investigated whether the induction of inducible nitric oxide synthase (iNOS) produced by acute exercise in rat skeletal muscle could be prevented by melatonin and whether iNOS down‐regulation was related to inhibition of nuclear factor kappaB (NF‐ κ B) activation. Male Wistar rats received melatonin i.p. at a dose of 1.0 mg/kg body weight 30 min before being exercised for 60 min on a treadmill at a speed of 25 m/min and a 10% slope. Exercise caused a significant induction of iNOS protein levels and a marked activation of NF‐ κ B that were significantly prevented in rats treated with melatonin. Exercise also resulted in increased I κ B kinase α (IKK α ) and phosphorylated I κ B α protein levels, whereas I κ B α content decreased. These effects were blocked by melatonin administration. The increase in the muscle concentration of thiobarbituric acid reactive substances and in the oxidized/reduced glutathione ratio induced by exercise was partially prevented by melatonin. Our data indicate that melatonin has potent protective effects against damage caused by acute exercise in rat muscle, preventing oxidative stress, NF‐ κ B activation and iNOS over‐expression. These findings support the view that melatonin treatment, by abolishing the IKK/NF‐ κ B signal transduction pathway, might block the production of noxious mediators involved in the inflammatory process.