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Protective Effects of Isorhamnetin against Hydrogen Peroxide-Induced Apoptosis in C2C12 Murine Myoblasts

  • Journal of Korean Medicine for Obesity Research
  • Abbr : J Korean Med Obes Res
  • 2015, 15(2), pp.93-103
  • Publisher : The Society of Korean Medicine for Obesity Research
  • Research Area : Medicine and Pharmacy > Korean Medicine
  • Published : December 30, 2015

Yung Hyun Choi 1

1동의대학교

Candidate

ABSTRACT

Objectives: It was investigated the cytoprotective efficacies of isorhamnetin, a flavonoidoriginally derived from Hippophae rhamnoides L., against oxidative stress-induced apoptosis inC2C12 myoblasts. Methods: The effects of isorhamnetin on cell growth, apoptosis and reactive oxygen species(ROS) generation were evaluated by trypan blue dye exclusion assay, 4',6-diamidino-2-phenylindolestaining and flow cytometry. The levels of apoptosis-regulatory and nuclear factorerythroid 2-related factor 2 (Nrf2) signaling pathway-related proteins, and caspase activities(caspase-3 and -9) were determined by Western blot analysis and colorimetric assay, respectively. Results: Our results revealed that treatment with isorhamnetin prior to hydrogen peroxide (H2O2)exposure significantly increased the C2C12 cell viability and, indicating that the exposure ofC2C12 cells to isorhamnetin conferred a protective effect against oxidative stress. Isorhamnetinalso effectively attenuated H2O2-induced apoptosis and ROS generation, which was associatedwith the restoration of the upregulation of Bax and downregulation of Bcl-2 induced by H2O2. Inaddition, H2O2 enhanced the activation of caspase-9 and -3, and degradation of poly (ADPribose)-polymerase, a typical substrate protein of activated caspase-3; however, these eventswere almost totally reversed by pretreatment with isorhamnetin. Moreover, isorhamnetinincreased the levels of heme oxygenase-1, a potent antioxidant enzyme, associated with theinduction of Nrf2. Conclusions: Our data indicated that isorhamnetin may potentially serve as an agent for thetreatment and prevention of muscle disorders caused by oxidative stress.

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