Conessine interferes with oxidative stress-induced C2C12 myoblast cell death through inhibition of autophagic flux

Hyunju Kim, Kang Il Lee, Minsu Jang, Sim Namkoong, Rackhyun Park, Hyunwoo Ju, Inho Choi, Won Keun Oh, Junsoo Park

Research output: Contribution to journalArticlepeer-review

11 Citations (Scopus)

Abstract

Conessine, a steroidal alkaloid isolated from Holarrhena floribunda, has anti-malarial activity and interacts with the histamine H3 receptor. However, the cellular effects of conessine are poorly understood. Accordingly, we evaluated the involvement of conessine in the regulation of autophagy. We searched natural compounds that modulate autophagy, and conessine was identified as an inhibitor of autophagic flux. Conessine treatment induced the formation of autophagosomes, and p62, an autophagic adapter, accumulated in the autophagosomes. Reactive oxygen species such as hydrogen peroxide (H2O2) result in muscle cell death by inducing excessive autophagic flux. Treatment with conessine inhibited H2O2-induced autophagic flux in C2C12 myoblast cells and also interfered with cell death. Our results indicate that conessine has the potential effect to inhibit muscle cell death by interfering with autophagic flux.

Original languageEnglish
Article numbere0157096
JournalPloS one
Volume11
Issue number6
DOIs
Publication statusPublished - 2016 Jun 1

Bibliographical note

Publisher Copyright:
© 2016 Kim et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

All Science Journal Classification (ASJC) codes

  • General Biochemistry,Genetics and Molecular Biology
  • General Agricultural and Biological Sciences
  • General

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