Promoting Effects And Mechanism Of Ginsenoside Rg1on Spinal Nerve Repair After Injury

Backgrounds:Spinal nerve injury is very common in the field of spinal surgery. There aremany reasons that might cause the spinal nerve being compressed, stretched orcrushed, resulting in different levels of motor dysfunction and sensorydysfunction. The life quality of patients is severely lowered. However, thetherapeutic effect of spinal nerve injury is not good. Spinal nerve injury is still aclinical challenge for surgeons.Spinal nerve injury belongs to the category of peripheral nerves injury. Atpresent, the research of Chinese herbal medicine and its extracts is one of hotresearch topics. The present research shows that, Ginsenoside Rg1(one ofginseng extracts) might have trophism and protective effects on the centralnervous system, and can inhibit apoptosis of neurons. Presumably, this kind ofneuro-protective effects of GRg1may also apply to the peripheral nervoussystem. But the current research about GRg1is focused mainly on brainprotection. The research about application of GRg1in peripheral nerve injuryand the mechanism has been rare. We presume that, the application of GRg1inperipheral nerve injury may promote the nerve regeneration.Objective: To determine whether GRg1can promote the nerve regeneration inperipheral nerve injury. In addition, to reveal the mechanism underlying thebeneficial effect of GRg1on peripheral nerve repair, further studies wereperformed to identify the effect of GRg1on the biological behaviors ofneuroglia cell of peripheral nerve system (Schwann cells, SCs) after injury.Materials and Methods:1. A model of sciatic nerve crush injury in rats was established. Differentdoses of GRg1were administrated (high/low dose). Mecobalamin or saline wasadministrated to the control groups. The nerve regeneration, functional recoveryand condition of the target organ were investigated by nerve morphometricanalysis, retrograde labeling, electrophysiological studies, behavioral tests ofstepping (The sciatic nerve function index, SFI), and histological appearance ofthe target muscles.2. A SCs oxidative damage model was established. GRg1wereadministrated after the oxidative damage. Mecobalamin or saline wasadministrated to the control groups. The oxidative damage level of the injuredSCs was investigated by examining the malondialdehyde (MDA) andsuperoxide dismutase (SOD) using spectrophotometer. The growth of injuredSCs was characterized using DAPI staining and a MTT assay. The apoptosis ofthe injured SCs was examined by a cell apoptosis assay using flow cytometer.The mRNA and protein levels of NGF and BDNF in injured SCs were assayedby RT-PCR and Western blotting, and the amount of NGF and BDNF secretedwas determined by an ELISA assay.Results:1. The nerve regeneration and functional recovery (nerve morphometricanalysis, retrograde labeling, electrophysiological studies) in the high-dose GRg1group were better than other groups. The sciatic nerve function index (SFI)and histological appearance of the target muscles recovered well in thehigh-dose GRg1group, which were the most close to the normal group.2. The level of oxidative damage and apoptosis in the GRg1group wassignificantly lower than control groups. The proliferation and vitality in theGRg1group were significantly better than control groups. In addition, theexpression and secretion of NGF and BDNF by the injured SCs in GRg1groupis significantly more than control groups and normal group.Conclusion:GRg1can effectively promote the nerve regeneration and functionalrecovery in peripheral nerve injury. At the same time, GRg1can reduce theoxidative damage on the injured SCs, promote the proliferation and vitality, andinhibit the apoptosis. The expression and secretion of NGF and BDNF by theinjured SCs were also significantly enhanced. The regulatory effect of GRg1oninjured SCs mentioned above might partially contribute to the beneficial effectof GRg1on nerve regeneration and functional recovery in peripheral nerveinjury.