Protective effects of ginsenoside Rg3 on TNF-α-induced human nucleus pulposus cells through inhibiting NF-κB...

Area of Science:

• Biochemistry
• Cell Biology
• Pharmacology

Background:

• Intervertebral disc degeneration is linked to nucleus pulposus cell (NPC) dysfunction.
• Tumor Necrosis Factor-alpha (TNF-α) induces apoptosis, oxidative stress, and alters extracellular matrix (ECM) metabolism in NPCs.
• Ginsenoside Rg3 is a bioactive compound with potential therapeutic properties.

Purpose of the Study:

• To investigate the protective effects of ginsenoside Rg3 against TNF-α-induced damage in human nucleus pulposus cells.
• To evaluate Rg3's impact on NPC apoptosis, proliferation, ECM metabolism, and oxidative stress.

Main Methods:

• Human NPCs were treated with TNF-α and varying concentrations of ginsenoside Rg3.
• Apoptosis and cell cycle were assessed using Annexin V-FITC/PI staining and flow cytometry.
• Cell proliferation was measured by CCK-8 assay.
• ECM gene expression (MMP3, ADAMTS5, Aggrecan, COL2A1) was analyzed via qRT-PCR, ELISA, and Western blotting.
• Oxidative stress markers (ROS, MDA, SOD, GSH-PX) and NF-κB/p65 pathway activation were evaluated.

Main Results:

• TNF-α significantly increased NPC apoptosis (Bax, Caspase-3 up; Bcl-2 down), inhibited proliferation, and arrested the cell cycle.
• TNF-α elevated ECM-degrading enzymes (MMP3, ADAMTS5), ROS, MDA, and NF-κB/p65 activation, while decreasing ECM synthesis genes (Aggrecan, COL2A1) and antioxidant enzymes (SOD, GSH-PX).
• Ginsenoside Rg3 treatment dose-dependently reversed these TNF-α-induced detrimental effects.

Conclusions:

• Ginsenoside Rg3 attenuates TNF-α-induced human NPC impairment.
• Rg3's protective mechanism involves blocking the NF-κB signaling pathway.
• Ginsenoside Rg3 shows potential as a therapeutic agent for intervertebral disc degeneration.