Ethanol extract of Prunus mume fruit attenuates hydrogen peroxide-induced oxidative stress and apoptosis involving Nrf2/HO-1 activation in C2C12 myoblasts

Revista Brasileira de Farmacognosia

Kim, Heui-Soo¹  Kim, Gi-Young¹  Institute of Hukyong Food, Busan, Republic of Korea¹  Kang, Ji Sook¹  Hwang, Hye Jin¹  Jeju National University, Jeju, Republic of Korea¹  Kim, Suhkmann¹  Busan National University, Yangsan, >Republic of Korea¹  Dongeui University, Republic of Korea¹  Kosin University, Busan, Republic of Korea¹  Park, Cheol¹  Kim, Cheol Min¹  Dongeui University, Busan, >Republic of Korea¹  Kim, Dong Joo¹  Choi, Yung Hyun¹  Dongeui University, Busan, Republic of Korea¹  Cha, Hee-Jae¹  Pusan National University, Busan, Republic of Korea¹  Kim, Byung Woo¹ 

关键词:  Prunus mume;    Oxidative stress;    DNA damage;    Apoptosis;    Nrf2/HO-1;   

DOI  :  10.1016/j.bjp.2015.06.012

来源: Sociedade Brasileira de Farmacognosia

【 摘 要 】

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.

【 授权许可】

Unknown