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Base Excision Repair01:54

Base Excision Repair

One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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Mechanism of ginsenoside Rb3 against OGD/R damage based on metabonomic and PCR array analyses.

Fuhui Li1, Jie Tao2, Mingmin Zhou1

  • 1College of Notoginseng Medicine, Wenshan University, Wenshan, Yunnan 663099, P.R. China.

Biomedical Reports
|October 18, 2024
PubMed
Summary

Ginsenoside Rb3 (G-Rb3) protects HT22 cells from oxygen-glucose deprivation/reoxygenation (OGD/R) injury by inhibiting apoptosis. This neuroprotective effect involves modulating metabolites and downregulating pro-apoptotic genes.

Keywords:
PCR arrayapoptosisginsenoside Rb3metabolomicsoxygen glucose deprivation/reoxygenation

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Metabolomics

Background:

  • Oxygen-glucose deprivation/reoxygenation (OGD/R) induces cell injury, particularly in neurons.
  • Ginsenoside Rb3 (G-Rb3) is a compound with potential therapeutic properties.
  • Understanding the protective mechanisms of G-Rb3 against OGD/R injury is crucial for developing neuroprotective strategies.

Purpose of the Study:

  • To investigate the protective effects of G-Rb3 against OGD/R-induced injury in HT22 cells.
  • To elucidate the underlying mechanisms of G-Rb3's action using metabolomics and PCR array analysis.

Main Methods:

  • HT22 cells were subjected to an in vitro OGD/R model.
  • Cell viability, apoptosis, and protein expression (Bax, Bcl-2, caspase-3) were assessed.
  • Metabolomic analysis identified differential metabolites.
  • PCR array identified differential gene expression.

Main Results:

  • G-Rb3 significantly reduced OGD/R-induced apoptosis and cell death.
  • G-Rb3 modulated apoptosis-related proteins (decreased Bax and caspase-3, increased Bcl-2).
  • Metabolomic analysis revealed alterations in pathways like galactose metabolism and citrate cycle, with changes in guanosine, enalaprilat, and sorbitol levels.
  • G-Rb3 downregulated pro-apoptotic genes including Trp63, Trp73, Dapk1, Casp14, and Cd70.

Conclusions:

  • G-Rb3 exhibits significant neuroprotective effects against OGD/R injury in vitro.
  • The mechanism involves apoptosis inhibition through metabolic pathway modulation and downregulation of specific pro-apoptotic genes.