Ginsenoside Rk3 Treats Corneal Injury Through the HMGB1/TLR4/NF-κB Pathway

The cornea serves as a vital protective shield for the eye, safeguarding its intricate internal structures from external threats. Damage to the cornea compromises this protective function, triggering inflammation and potentially causing long-term harm. While ginsenoside Rk3 has demonstrated potential for repairing the corneal barrier and reducing inflammation, its effectiveness in treating corneal damage remains relatively unexplored. This comprehensive study uses both in vivo and in vitro models to investigate the therapeutic capabilities of ginsenoside Rk3. Using two models of corneal damage, a benzalkonium chloride-induced mouse model and a high osmolarity-induced human corneal epithelial cell model, we scrutinized the effects of ginsenoside Rk3 treatment. Our results showed that ginsenoside Rk3-treated mice manifested reduced corneal damage and inflammation compared with their untreated counterparts. Furthermore, mice treated with ginsenoside Rk3 exhibited an organized arrangement of corneal cells and diminished stromal layer thickness, indicating reparative properties of ginsenoside Rk3. Additionally, ginsenoside Rk3 increased the expression of tight junction proteins, suppressed inflammatory factors, and decreased HMGB1 protein expression, thereby modulating downstream signaling pathways. Collectively, our findings present compelling evidence that ginsenoside Rk3 is a promising therapeutic option for corneal injury. By repairing the corneal barrier, mitigating inflammation, and modulating specific protein levels, ginsenoside Rk3 opens new avenues for managing corneal damage.