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The effect of the K ATP channel opener Nicorandil in lipid‐peroxidation in skeletal muscle atrophy
Author(s) -
PADILLAMALDONADO PAULINA,
SANCHEZDUARTE ELIZABETH,
GÓMEZBARROSO MARIANA,
SANCHEZPEREZ ALINA,
CORTESROJO CHRISTIAN,
SAAVEDRAMOLINA ALFREDO,
MONTOYAPEREZ ROCIO
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.618.23
Subject(s) - nicorandil , atrophy , muscle atrophy , tbars , medicine , chemistry , skeletal muscle , mitochondrion , endocrinology , atp sensitive potassium channel , lipid peroxidation , oxidative stress , biochemistry , glibenclamide , diabetes mellitus
Muscle atrophy is defined as a decrease muscle tissue size due to cellular shrinkage caused by loss of organelles, cytoplasm and proteins. The main characteristic of this pathology is the increase in protein degradation and a decrease in protein re‐synthesis. It has been documented that the mitochondrial ATP sensitive potassium channel (mitoK ATP ), is involved in the resistance of the muscle fatigue and recovery from ischemia‐reperfusion injury and protection during atrophy process; Nicorandil has been described as a selective mitoK ATP opener which confers protection to muscle during stressful conditions, the aim of this study was to determine the protective effect of Nicorandil over the damage caused by atrophy. C57BL/6 male mice 14–16 weeks‐old were used for the experimental basis; these animals were separated into 4 groups: 1) Control, 2) Nicorandil, 3) Atrophy and 4) Atrophy treated with Nicorandil. Atrophy was induced by hindlimb unloading by the tail method. Nicorandil was purveying in 40 mg/kg doses by intramuscular injection during 14 days. Once finished the treatment, the animals were sacrificed by cervical dislocation and the hindlimb were used for mitochondria isolation, once obtained the isoled mitochondria the lipid‐peroxidation was measured by the TBARS method. This reaction was measured in a Spectrophotometer Perkin Elmer Lambda 18 UV/VIS in ʎ of 523 nm. The results were for the group Nicorandil was higher against the Control group 50.5827%, the Atrophy group was 53.03% against the Control group, and the Nicrandil+Atrophy group had an increase in the activity against the Control group. Lipid‐peroxidation had been used as a marker of oxidative stress, as we know, this has been stablished that atrophy leads to an accumulation of toxic substances as reactive oxygen species, like we observe here the Nicorandil treatment has no effect in healthy mice but the opening of this channel downregulates lipid oxidation in the atrophied that can give us a thought of cytoprotection. Support or Funding Information RMP‐CIC2017 This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .