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Natural compound methyl protodioscin protects rat brain from ischemia/reperfusion injury through regulation of

Shu Guo1, Yi-Yue Zhang2, Jing-Jie Peng3

  • 1Department of Laboratory Medicine, The Third Xiangya Hospital of Central South University, Changsha 410013, China; Department of Pharmacology, Xiangya School of Pharmaceutical Sciences, Central South University, Changsha 410078, China.

European Journal of Pharmacology
|February 5, 2019
PubMed

Insights

Methyl protodioscin (MPD) protects against brain ischemia/reperfusion (I/R) injury by regulating the Mul1/SOD2 pathway. MPD treatment reduces neurological deficits and infarct volume by modulating mitochondrial E3 ubiquitin ligase 1 (Mul1) and superoxide dismutase 2 (SOD2) levels.

Area of Science:

  • Neuroscience
  • Mitochondrial Biology
  • Pharmacology

Background:

  • Methyl protodioscin (MPD) shows potential in treating cardiovascular conditions.
  • Mitochondrial E3 ubiquitin ligase 1 (Mul1) is crucial for mitochondrial health.
  • Cerebral ischemia/reperfusion (I/R) injury involves mitochondrial dysfunction.

Purpose of the Study:

  • To investigate the neuroprotective effects of MPD against cerebral I/R injury.
  • To explore the role of the Mul1/superoxide dismutase 2 (SOD2) pathway in MPD's protective mechanism.

Main Methods:

  • In vivo study using Sprague-Dawley rats subjected to middle cerebral artery occlusion.
  • In vitro study using cultured HT22 cells exposed to hypoxia-reoxygenation (H/R).
  • Assessment of neurological deficit scores, infarct volume, cell apoptosis, LDH release, Mul1 and SOD2 protein levels, and reactive oxygen species generation.

Main Results:

  • MPD treatment significantly attenuated I/R injury in rats, reducing neurological deficits and infarct volume.
  • MPD protected HT22 cells from H/R-induced injury, decreasing apoptosis and LDH release.
  • MPD modulated the Mul1/SOD2 pathway, decreasing Mul1 and increasing SOD2 expression, thereby reducing reactive oxygen species.

Conclusions:

  • Upregulation of Mul1 contributes to cerebral I/R injury by suppressing SOD2.
  • MPD exerts neuroprotection against cerebral I/R injury via the Mul1/SOD2 pathway.
  • MPD represents a potential therapeutic agent for cerebral I/R injury.
Keywords:
Brain injuryIschemia/reperfusionMethyl protodioscinMitochondrial E3 ubiquitin ligase 1Superoxide dismutase 2

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