Open AccessEthanol extract of Prunus mume fruit attenuates hydrogen peroxide-induced oxidative stress and apoptosis involving Nrf2/HO-1 activation in C2C12 myoblasts
Author(s) -
Ji Sook Kang,
Dong-Joo Kim,
GiYoung Kim,
HeeJae Cha,
Suhkmann Kim,
HeuiSoo Kim,
Cheol Park,
Hye Jin Hwang,
Byung Woo Kim,
Cheol Min Kim,
Yung Hyun Choi
Publication year - 2016
Publication title -
revista brasileira de farmacognosia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.432
H-Index - 46
eISSN - 1981-528X
pISSN - 0102-695X
DOI - 10.1016/j.bjp.2015.06.012
Subject(s) - reactive oxygen species , oxidative stress , c2c12 , apoptosis , chemistry , mitochondrion , dna damage , inner mitochondrial membrane , oxidative phosphorylation , biochemistry , microbiology and biotechnology , myocyte , biology , myogenesis , dna
The fruit of the Prunus mume (Siebold) Siebold & Zucc., Rosaceae (Korean name: Maesil) has long been used as a health food or valuable medicinal material in traditional herb medicine in Southeast Asian countries. In this study, we determined the potential therapeutic efficacy of the ethanol extract of P. mume fruits (EEPM) against H2O2-induced oxidative stress and apoptosis in the murine skeletal muscle myoblast cell line C2C12, and sought to understand the associated molecular mechanisms. The results indicated that exposure of C2C12 cells to H2O2 caused a reduction in cell viability by increasing the generation of intracellular reactive oxygen species and by disrupting mitochondrial membrane permeability, leading to DNA damage and apoptosis. However, pretreatment of the cells with EEPM before H2O2 exposure effectively attenuated these changes, suggesting that EEPM prevented H2O2-induced mitochondria-dependent apoptosis. Furthermore, the increased ex-pression and phosphorylation of nuclear factor erythroid 2-related factor 2 (Nrf2) and up-regulation of heme oxygenase-1 (HO-1), a phase II antioxidant enzyme, were detected in EEPM-treated C2C12 cells. We also found that zinc protoporphyrin IX, an HO-1 inhibitor, attenuated the protective effects of EEPM against H2O2-induced reactive oxygen species accumulation and cytotoxicity. Therefore, these results indicate that the activation of the Nrf2/HO-1 pathway might be involved in the protection of EEPM against H2O2-induced cellular oxidative damage. In conclusion, these results show that EEPM contributes to the prevention of oxidative damage and could be used as a nutritional agent for oxidative stress-related diseases