DOI QR코드

DOI QR Code

Protective Effect of Root of Vitis Amurensis Extract Against Oxidative Stress-Induced Cytotoxicity in C2C12 Myogenic Cells

C2C12 근원세포에서 산화적 스트레스 유발 세포 독성에 대한 머루근 추출물의 보호 효과

  • Su-Eun Jung (Department of Korean Medicine Rehabilitation, Dong-Eui University Korean Medicine Hospital) ;
  • Sung-Woo Cho (Department of Korean Medicine Rehabilitation, Dong-Eui University Korean Medicine Hospital) ;
  • Song-Mi Park (Department of Korean Medicine Rehabilitation, Dong-Eui University Korean Medicine Hospital) ;
  • Yung-Hyun Choi ( Department of Biochemistry, College of Korean Medicine, Dong-Eui University)
  • 정수은 (동의대학교 한방병원 한방재활의학과) ;
  • 조성우 (동의대학교 한방병원 한방재활의학과) ;
  • 박송미 (동의대학교 한방병원 한방재활의학과) ;
  • 최영현 (동의대학교 생화학교실)
  • Received : 2026.06.04
  • Accepted : 2026.06.29
  • Published : 2026.07.30

Abstract

Objectives This study evaluated the protective effects of water extract of Vitis amurensis root (WEVA) against hydrogen peroxide H2O2-induced oxidative damage in C2C12 myoblasts. Methods To evaluate the protective effects of WEVA, C2C12 myoblasts were treated with H2O2 in the presence or absence of WEVA. The effects on cell viability, reactive oxygen species (ROS) generation, DNA damage, apoptosis, and mitochondrial function were analyzed using specific biochemical assays and western blotting. The involvement of the nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway was further investigated using a specific HO-1 inhibitor. Results Our results demonstrated that WEVA protected against H2O2-induced reduction in cell viability and DNA damage, while simultaneously inhibiting the production of ROS. WEVA attenuated H2O2-induced apoptosis in C2C12 cells by increasing the Bcl-2/Bax expression ratio, inhibiting caspase-3 activation, and blocking the cleavage of poly(ADP-ribose) polymerase. Furthermore, WEVA reduced the release of cytochrome c from the mitochondria to the cytosol by preventing mitochondrial membrane disruption in H2O2-treated C2C12 cells. Under oxidative stress, WEVA enhanced the expression and activity of HO-1, a process mediated by the induction and phosphorylation of Nrf2. However, the ROS scavenging and ytoprotective effects of WEVA were significantly diminished by an HO-1 inhibitor, indicating that WEVA prevents oxidative damage in C2C12 myoblasts by promoting Nrf2-mediated HO-1 activity. Conclusions In conclusion, these findings suggest that WEVA, as an Nrf2 activator, possesses ROS scavenging capabilities and holds potential for protecting against oxidative stress-mediated muscle diseases.

Keywords