PACAP对大鼠创伤性脑损伤后caspase-3的影响

Effect of pituitary adenylate cyclase-activating polypeptide on caspase-3 following traumatic brain injury in rats

目的观察垂体腺苷酸环化酶激活肽(PACAP)对创伤性颅脑损伤(TBI)后大鼠脑组织内切冬酶-3(caspase-3)表达及活性变化的影响。方法采用TBI模型,运用免疫组织化学及免疫荧光技术,观察TBI伤后2h～3d伤侧大脑皮层、海马caspase-3表达及活性变化情况。结果在伤后各时相点(2、12、24、48、72h)PACAP治疗组caspase-3表达与TBI组相比较,皮质与海马的表达都要相对减少;caspase-3的活性明显下降(P<0.05)。结论PACAP能降低TBI脑组织内caspase-3表达及活性,减少神经细胞凋亡。

Objective To investigate the changes of caspase-3 in brain tissue of rats following traumatic brain injury （TBI） and the effects of low dose pituitary adenylate cyclase-activating polypeptide （PACAP） by intracerebroventricular administration on it. Methods Based upon TB model the expression of caspase-3 protein was detected by immunohistochemistry and the activity of caspase-3 was detected with caspase-3 fluorescent assay kit in injured cortex and hippocampus at the second hour to the third day after medium traumatic brain injury. Results The levels of caspase-3 positive neurons and terminal deoxynucleotide transferase mediated biotinglated deoxyuridine triphosphate nick end labeling （TUNEL） positive neurons and the activity of caspase-3 in the injuried cortex and hippocampus after treatment with low-dose PACAP decreased significantly compared with the control group in every time point （2 h, 12 h, 24 h, 48 h, 72 h） （P 〈0.05）. Conclusion The treatment of lowdose PACAP can reduce the activity of caspase-3 and protect neurons from apoptotic death caused by acute TBI.