[Ginsenoside Rg1 may protect SHSY5Y cells from apoptosis induced by MPP+ through JNK way]

Fang Fang1, Xiao-chun Chen, Yuan-gui Zhu

  • 1Fujian Institute of Geriatrics, Affiliated Union Hospital, Fujian Medical University, Fuzhou 350001, China.

Abstract

Insights

Ginsenoside Rg1 protects SHSY5Y cells from 1-methyl-4-phenylpyridinium (MPP+)-induced apoptosis. This neuroprotection involves reducing reactive oxygen species (ROS), inhibiting c-jun NH2-terminal kinase (JNK) activity, and decreasing cleaved Caspase-3 expression.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Cell Biology

Background:

  • MPP+ induces apoptosis in SHSY5Y cells, a model for Parkinson's disease.
  • Ginsenoside Rg1 is a compound with potential neuroprotective properties.

Purpose of the Study:

  • To investigate the mechanism by which ginsenoside Rg1 protects against MPP+-induced apoptosis.
  • To explore the role of reactive oxygen species (ROS) and c-jun NH2-terminal kinase (JNK) signaling in this protective effect.

Main Methods:

  • Apoptosis was assessed using AO-EB staining and flow cytometry.
  • ROS levels were quantified by flow cytometry.
  • JNK activity and cleaved Caspase-3 expression were detected using Western Blotting and immunocytochemistry, respectively.

Main Results:

  • MPP+ treatment significantly increased apoptosis, ROS levels, JNK activity, and cleaved Caspase-3 expression in SHSY5Y cells.
  • Pretreatment with ginsenoside Rg1 (10 µmol/L) or N-acetylcysteine (NAC, 2.5 mmol/L) attenuated MPP+-induced apoptosis.
  • Rg1 and NAC pretreatment reduced ROS levels, JNK activity, and cleaved Caspase-3 expression compared to MPP+ alone.

Conclusions:

  • Ginsenoside Rg1 exhibits neuroprotective effects against MPP+-induced apoptosis in SHSY5Y cells.
  • The protective mechanism is associated with the reduction of ROS, inhibition of JNK signaling pathway, and decreased cleaved Caspase-3 expression.

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