Gene therapy for traumatic brain injury with A20 in rats

Objective To investigate the anti-apoptotic effect of gene A20 in treatment of trau-matic brain injury (TBI). Methods Thirty-five Sprague-Dawley rats were made severe TBI models and assigned randomly to experimental group and control group (35 rats in each group). After severe TBI, the rats in experimental group were injected with liposome-pcDNA3.1-A20 and those in control group injected with liposome pcDNA3.1-A20 at 30 minutes after severe TBI. The animals in both groups were sacrificed to remove the brain of five rats from each group at 12, 24, 48, 72 and 168 hours for sec-tioning. The expression of A20 and neurocyte apoptosis were defined by immunohistological method and TUNEL accordingly. The other ten rats were testified for neurological function at 1,2, 3 and 4 weeks af-ter TBI. Results The expression of A20 in experimental group was higher than that in control group, with statistical differences (P < 0. 01). The peak neurocyte apoptosis was found at 72 hours after TBI. The number of apoptosis cells in experimental group was lower than that in control group at 12, 24, 48 and 72 hours afte TBI (P < 0.01 or 0.05). At the 4th week after TBI, the neurological function in exper-imental group was better than that in control group (P < 0.05). Conclusion Gene therapy with A20 may have anti-apoptosis effect and exert neuroprotective effect on severe TBI. Key words: Gene, A20;  Brain injuries;  Apoptosis