Study On Effect Of Ligustrazine(LZ) On Apoptosis Of Neuron And Expression Of Bcl-2 Bax Gene After Severe Brain Injury (SBI) In Rats

Objective: To investigate the expression of Bcl-2,Bax gen and apoptosis in the rat brain following severe brain injury(SBI) and evaluate neuroprotecting effects of Ligustrazine (LZ) .Methods: 120 SD rats were randomly assigned into three groups: pseudo-operation group,model group and (LZ)treatment group. Every group contained 40 rats. SBI was established according to Feeney's method. The treatment group was administrated with LZ (20mg/KG.d) transperitoneally. Rats were killed at 7h,24h,72h,168h after SBI. TUNEL(terminal deoxynucleotide transferase mediated nick end labeling)and immunohistochemistry were used to detect apoptosis and Bcl-2,Bax expression in all the brain tissue.Result: (1)The immunoreactivity of Bcl-2 protein decreased in the penumbra after SBI,while the Bax protein expression increased significantly.(2)After SBI,the expression of Bcl-2 or Bax protein increased in model group compared with pseudo-operation group.the expression of Bcl-2 protein increased and Bax protein decreased significantly in LZ group compared with model group.(3)There are no or few the number of TUNEL positive cells in the pseudo-operation group, The number of TUNEL positive cells inthe treated(LZ) group is less than that of the model group.Conclusion: According to this date ,there are neuronal apoptosis and changeof Bcl-2,Bax protein expression. LZ could reduce the apoptosis of neuronafter severe brain injury through the improving express of Bcl-2 protein andinhibiting express of Bax protein,which might be one of mechanisms of LZtreating SBI.