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Mitochondrial dynamics and protective effects of a mitochondrial division inhibitor, Mdivi-1, in

Songyun Deng1, Yuhang Ai1, Hua Gong1

  • 1Department of Critical Care Medicine, Xiangya Hospital, Central South University, Changsha, 410008, PR China.

Biochemical and Biophysical Research Communications
|February 4, 2018
PubMed

Insights

Mdivi-1 treatment reduced brain damage and neuronal death in rats with sepsis-associated encephalopathy (SAE). This protective effect is linked to Mdivi-1

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Sepsis-associated encephalopathy (SAE) is a common and severe neurological complication of sepsis, often leading to mortality in Intensive Care Units.
  • Currently, there is no universally accepted treatment for SAE, highlighting the urgent need for therapeutic strategies.
  • SAE pathogenesis involves complex mechanisms, including oxidative stress and mitochondrial dysfunction, which contribute to neuronal damage.

Purpose of the Study:

  • To investigate the therapeutic potential of Mdivi-1, a dynamin-related GTPase (Drp1) inhibitor, in a rat model of SAE.
  • To elucidate the underlying mechanisms by which Mdivi-1 exerts neuroprotective effects in SAE.
  • To explore mitochondrial dynamics as a potential therapeutic target for SAE.

Main Methods:

  • Rats were induced with SAE and treated with Mdivi-1.
  • Brain damage was assessed using Nissl staining and TUNEL assay.
  • Plasma levels of S100 calcium binding protein B (S100B) and neuron-specific enolase (NSE) were measured.
  • Biochemical analyses and Western blot were performed to evaluate oxidative stress and mitochondrial dynamics markers, including Drp1, phosphorylated Drp1 (p-Drp1), and optic atrophy 1 (OPA1).

Main Results:

  • Mdivi-1 treatment significantly ameliorated brain damage and reduced the number of TUNEL-positive cells in the hippocampus.
  • Mdivi-1 inhibited the release of S100B and NSE into plasma, indicating reduced neuronal injury.
  • Mdivi-1 protected the hippocampus against oxidative stress.
  • Western blot analysis revealed that Mdivi-1 inhibited the increase in Drp1 and attenuated the decrease in OPA1 and p-Drp1 induced by lipopolysaccharide (LPS).

Conclusions:

  • Mdivi-1 demonstrates significant neuroprotective effects against SAE in a rat model.
  • The protective mechanisms involve the inhibition of Drp1, modulation of p-Drp1 and OPA1 levels, and mitigation of oxidative stress.
  • Mitochondrial dynamics represent a promising pharmacological target for the treatment of SAE.
Keywords:
Drp1Mdivi-1Mitochondrial dynamicsOPA1Oxidative stressSepsis-associated encephalopathy

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