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Drp1-associated mitochondrial dysfunction and mitochondrial autophagy: a novel mechanism in triptolide-induced

Muhammad Hasnat1, Ziqiao Yuan1, Muhammad Naveed2

  • 1Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing, 210009, China.

Cell Biology and Toxicology
|December 14, 2018
PubMed

Insights

Triptolide causes liver damage by disrupting mitochondria and triggering mitophagy. Targeting mitochondrial fission and autophagy may offer new therapeutic strategies for triptolide-induced hepatotoxicity.

Area of Science:

  • * Pharmacology and Toxicology
  • * Cellular Biology and Biochemistry
  • * Molecular Medicine

Background:

  • * Triptolide, from Tripterygium wilfordii, is known to cause severe hepatotoxicity.
  • * Previous research identified triptolide-induced mitochondrial toxicity in hepatocytes.
  • * The precise biomolecular mechanisms underlying triptolide-induced mitochondrial dysfunction remain unclear.

Purpose of the Study:

  • * To investigate the link between mitochondrial fragmentation and mitophagy in triptolide-induced hepatotoxicity.
  • * To elucidate the molecular pathways involved in triptolide's effects on mitochondrial dynamics.
  • * To explore potential therapeutic targets for mitigating triptolide-induced liver injury.

Main Methods:

  • * In vitro studies using L02 cells to assess mitochondrial function, ROS production, ATP levels, and mitochondrial DNA copy number.
  • * Analysis of mitochondrial dynamics and expression of the fission protein Drp1 (dynamin-related protein 1).
  • * In vivo studies using rat liver tissues and transmission electron microscopy, with and without Mdivi-1 treatment.

Main Results:

  • * Triptolide induced concentration-dependent ROS production, decreased mitochondrial depolarization, reduced ATP generation, and declined mitochondrial DNA copy number.
  • * Triptolide caused mitochondrial fragmentation and disturbed mitochondrial dynamics, linked to increased Drp1 expression.
  • * Increased colocalization of lysosomes and autophagosomes with mitochondria indicated mitophagy activation, which was inhibited by Mdivi-1.

Conclusions:

  • * Mitochondrial fission-associated mitophagy is a novel mechanism contributing to triptolide-induced hepatotoxicity.
  • * Targeting mitochondrial fission and the mitochondrial autophagy signaling pathway presents a potential therapeutic strategy for triptolide-induced liver injury.
Keywords:
Drp1HepatotoxicityMitochondrial fragmentationMitophagyTriptolide

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