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Neuroprotective Effect of SCM-198 through Stabilizing Endothelial Cell Function.

Qiu-Yan Zhang1,2, Zhi-Jun Wang2,3, Lei Miao4

  • 1Yantai Institute of Materia Medica, Yantai Branch, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, China.

Oxidative Medicine and Cellular Longevity
|December 13, 2019
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Summary

SCM-198, derived from Herba leonuri, offers neuroprotection against ischemic stroke by reducing neuronal damage and oxidative stress. It activates the p-STAT3/NOX4/Bcl-2 pathway, suggesting potential therapeutic use.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Ischemic stroke causes irreversible neuronal damage and is a leading cause of death.
  • Leonurine (SCM-198), from Herba leonuri, shows promise for cardiovascular and brain diseases.
  • Understanding SCM-198's neuroprotective mechanisms is crucial for developing stroke treatments.

Purpose of the Study:

  • To investigate the therapeutic potential of SCM-198 against post-ischemic neuronal injury.
  • To elucidate the underlying molecular mechanisms of SCM-198's neuroprotective effects.
  • To evaluate SCM-198's impact on oxidative stress and apoptosis in neuronal injury models.

Main Methods:

  • Established transient middle cerebral artery occlusion (tMCAO) rat models and oxygen-glucose deprivation/re-oxygenation (OGD/R) cell models.
  • Utilized transmission electron microscopy (TEM), Nissl staining, and Fluoro-Jade B (FJB) staining for neuronal assessment.
  • Performed cell viability assays, biochemical analyses (MDA, CAT), apoptosis detection (TUNEL), Western blotting, immunofluorescence, and co-immunoprecipitation to study the p-STAT3/NOX4/Bcl-2 pathway.

Main Results:

  • SCM-198 treatment improved neuron morphology, reduced cell loss, and decreased degenerating neurons in tMCAO rats.
  • In OGD/R models, SCM-198 enhanced cell viability, restored CAT activity, improved SOD1 expression, and reduced MDA levels.
  • SCM-198 inhibited apoptosis, upregulated anti-apoptotic proteins (Bcl-2, Bcl-xl), downregulated pro-apoptotic Bax, and activated the p-STAT3/NOX4/Bcl-2 signaling pathway.

Conclusions:

  • SCM-198 demonstrates significant neuroprotective effects against ischemic injury in both in vivo and in vitro models.
  • The mechanism involves mitigating oxidative stress and apoptosis via the p-STAT3/NOX4/Bcl-2 signaling pathway.
  • SCM-198 shows potential as a therapeutic agent for neuroprotection by stabilizing endothelial cell function.