Ginsenoside Rd promotes endogenous neurogenesis after traumatic brain injury and related mechanims

Objective To investigate the effect of ginsenoside Rd (GSRd) on endogenous neurogenesis after traumatic brain injury (TBI) and the possible mechanisms involved. Methods Male SD rats were randomly divided into three groups: a sham group, a solvent group, and a GSRd group. A TBI model was established using a hydraulic injury device, and GSRd was injected via the tail vein. The Morris water maze test was used to assess learning and memory abilities in rats. Oxidative stress levels were detected using ROS, MDA, and SOD detection kits. Mitochondrial damage in the cortical cells of the injured area was detected by qPCR. Apoptosis in the cortical cells of the injured area was examined by TUENL kits. The levels of doublecortin(DCX) in the hippocampal tissue were measured by Western blot. Newly formed neurons in the cortical injury region were examined by NeuN/BrdU immunofluorescence. Results Compared with solvent group, the GSRd group showed a significant decrease in escape latency and a significant increase in the number of platform crossings (P<0.05). ROS and MDA levels were significantly reduced, while SOD activities were significantly enhanced (P<0.05). GSRd treatment inhibited the reduction in mitochondrial DNA copy number in cortical cells, relieved apoptosis in the injured cortical region, and increased neurogenesis in the injured hippocampus and cortex (P<0.05). Conclusions GSRd promotes endogenous neurogenesis and improves the recovery of learning and memory abilities in TBI rats, which may be related to inhibiting oxidative stress, mitochondrial damage, and reducing cell apoptosis.