Ginsenoside Rb1 inhibits neuronal apoptosis and damage, enhances spinal aquaporin 4 expression and improves neurological deficits in rats with spinal cord ischemia‑reperfusion injury.

Ginsenoside Rb1 is a potential therapeutic agent for the treatment of spinal cord ischemia‑reperfusion injury (SCII), although it has not yet been investigated in depth. The aim of the present study was to investigate the effects of ginsenoside Rb1 treatment on SCII and aquaporin‑4 (AQP4) expression in the rat spinal cord. Experimental animals were subjected to one of four conditions, including the blank control condition, sham procedure, spinal cord ischemia‑reperfusion induced by abdominal aortic occlusion or spinal cord ischemia‑reperfusion followed by ginsenoside Rb1 treatment. Locomotor activity was evaluated using the Basso Beattie Bresnahan scale. Spinal cord damage was assessed with hematoxylin and eosin and Nissl staining and the apoptotic rate was measured using terminal deoxynucleotidyl transferase dUTP nick end labeling. AQP4 expression was assessed by immunohistochemical analysis, western blotting and reverse transcription‑quantitative polymerase chain reaction. Abdominal aortic occlusion resulted in the reduced expression of AQP4 in the spinal cord, which gradually recovered over time. Furthermore, ginsenoside Rb1 treatment significantly attenuated this decrease and protected the integrity of and reduced the apoptotic rate in spinal cord neurons. Treatment with ginsenoside Rb1 attenuated the initial downregulation and advanced the recovery of AQP4 expression levels, suggesting a possible mechanism for the therapeutic effects on SCII.