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Mitochondrial Division Inhibitor 1 Attenuates Mitophagy in a Rat Model of Acute Lung Injury

Xu Luo1, Ruimeng Liu2, Zhihao Zhang2

  • 1Department of Critical Care Medicine, People's Hospital of Longhua, Shenzhen 518109, China.

Biomed Research International
|June 18, 2019
PubMed

Insights

Mdivi-1, an inhibitor of mitophagy, ameliorated acute lung injury (ALI) by reducing inflammation, apoptosis, and oxidative stress. This suggests inhibiting mitophagy may be a potential therapy for ALI.

Area of Science:

  • Cell Biology
  • Pathology
  • Pharmacology

Background:

  • Mitophagy regulates mitochondrial degradation.
  • The role of Mdivi-1 and mitophagy in acute lung injury (ALI) is not fully understood.
  • Mitochondrial dysfunction and cell damage can result from mitophagy.

Purpose of the Study:

  • To investigate the role of Mdivi-1, a mitophagy inhibitor, in ALI pathogenesis.
  • To determine if Mdivi-1 affects mitophagy activation in ALI.
  • To evaluate Mdivi-1's protective effects against LPS-induced ALI.

Main Methods:

  • Mdivi-1 treatment in LPS-induced ALI rat model.
  • Histopathological examination (HE staining).
  • Assessment of pulmonary microvascular permeability, wet/dry weight ratio, and oxygenation index (PaO2/FiO2).
  • Western blot analysis of mitophagy-related proteins.
  • Evaluation of mitochondrial dysfunction, apoptosis, oxidative stress, and inflammation markers in lung tissues and A549 cells.

Main Results:

  • Mdivi-1 treatment ameliorated ALI symptoms and lung injury.
  • Mdivi-1 inhibited LPS-induced mitophagy activation.
  • Mdivi-1 protected A549 cells from LPS-induced mitochondrial dysfunction.
  • Mdivi-1 reduced pulmonary cell apoptosis, oxidative stress, and inflammation in ALI rats.
  • Mdivi-1 mitigated inflammatory response and cell recruitment in the lungs.

Conclusions:

  • Mdivi-1 mitigates LPS-induced apoptosis, oxidative stress, and inflammation in ALI.
  • These protective effects are potentially linked to the inhibition of mitophagy.
  • Inhibiting mitophagy with Mdivi-1 may offer a potential therapeutic strategy for ALI.

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