Ginsenoside Rg1 controls CKLF1-mediated apoptosis to reduce hypoxic/reoxygenation injury in HT22 cells

Area of Science:

• Neuroscience
• Cell Biology
• Pharmacology

Background:

• Stroke is a leading cause of neurodegeneration.
• Ginsenoside Rg1 exhibits neuroprotective effects.
• Chemokine-like factor 1 (CKLF1) is upregulated in ischemic stroke and presents a potential therapeutic target.

Purpose of the Study:

• To investigate if Ginsenoside Rg1 (Rg1) can protect against oxygen-glucose deprivation/reoxygenation (OGD/R)-induced apoptosis in HT22 cells.
• To determine if Rg1 modulates chemokine-like factor 1 (CKLF1) expression in this model.
• To assess Rg1's effect on oxidative stress and neuroinflammation.

Main Methods:

• Established an OGD/R model in HT22 cells using sodium dithionite (Na2S2O4).
• Assessed Rg1's effects on cell viability, oxidative stress markers (LDH, MDA, CAT, SOD), and apoptosis (TUNEL staining, Western blotting for apoptosis-related proteins).
• Utilized a Transwell co-culture system with HT22 and BV-2 cells to evaluate Rg1's impact on microglia activation and inflammatory markers (NO, IL-1β).

Main Results:

• Rg1 treatment significantly reduced OGD/R-induced cell damage, oxidative stress, and apoptosis in HT22 cells.
• Rg1 dose-dependently downregulated CKLF1 expression and inhibited the activation of apoptotic proteins like Caspase-3.
• In co-culture systems, Rg1 suppressed microglia activation and the release of inflammatory mediators (NO, IL-1β).

Conclusions:

• Ginsenoside Rg1 attenuates OGD/R injury in HT22 cells by inhibiting CKLF1 expression, reducing oxidative stress and apoptosis.
• Rg1 also alleviates the inflammatory response in activated microglia (BV-2 cells).
• These findings highlight Rg1's therapeutic potential for stroke treatment.