Effect of rosiglitazone on neurofunction recovery after spinal cord injury in rats

English Keywords:Spinal cord injury  Rosiglitazone  NF-κB  Apoptosis  Caspase-3  Bcl-2  Rat

English Abstract:

  【Abstract】 Objective：To investigate the effect and mechanism of rosiglitazone on neurofunction recovery after spinal cord injury（SCI） in rats.Method：SCI model at T10 from 75 Sprague Dawley（SD） rats was induced by modified Allen method.All rats were divided into 3 groups：group B（n=25，rosiglitazone were injected at 5min，6h，24h after SCI），group C（n=25，rosiglitazone were injected as well as group B and G3335 were injected at 1h before the rosiglitazone were injected），and group A was sham control group（n=25，the same dose of normal saline were injected）.The BBB scoring system was employed to evaluate the behavioral changes of each group （n=6） at 1d，7d，2w，4w，6w after SCI.The protein expression of nuclear factor kappa-light-chain-enhancer of activated B cells（NF-κB） of each group（n=3） was observed by immunohistochemistry at 3d after SCI，and the total protein of each group was extracted for detection of expression of caspase-3 and Bcl-2 at 1d，3d，5d，7d，2w after SCI（n=3，each group at every time point）.Result：The BBB score of each group was 0 at 1d and 7d，while the BBB scores of group B were higher than that of group A and C at 4w after SCI，which showed significant difference between group B and the other two groups at 4w and 6w after SCI（P<0.05）.The expression of NF-κB protein were positive in every group，but the average optical density（AOD） of NF-κB protein in group B was lower than that of group A and C（P<0.05），which showed no significant difference between group A and C（P>0.05）.The expression of caspase-3 in group B was lower than that of group A and C（P<0.05），the expression of Bcl-2 in group B was higher than that of the other two groups（P<0.05），and the difference reached peak at 5d，there were no significant difference between group A and C at each time point.Conclusion：Rosiglitazone can promote the neurofunction recovery after spinal cord injury through inhibition of inflammation reaction and process of apoptosis.