自体嗅黏膜移植联合β-七叶皂甙钠干预脊髓损伤大鼠基质金属蛋白酶2、9的表达

背景:脊髓损伤后基质金属蛋白酶2、9的过表达与脊髓组织的继发性损伤有关。目的:观察自体嗅黏膜移植联合β-七叶皂甙钠干预脊髓损伤大鼠脊髓组织内基质金属蛋白酶2、9的表达与动物神经功能的恢复情况。方法:制作半横断脊髓损伤大鼠模型,随机分为4组,分别于腹腔注射β-七叶皂甙钠或生理盐水,以及损伤处植入自体嗅黏膜。结果与结论:干预后7,14d自体嗅黏膜组、β-七叶皂甙钠组、自体嗅黏膜联合β-七叶皂甙钠组BBB评分均高于模型对照组(P<0.05),自体嗅黏膜联合β-七叶皂甙钠组BBB评分高于自体嗅黏膜组、β-七叶皂甙钠组(P<0.05)。干预后1,3,7,14d自体嗅黏膜联合β-七叶皂甙钠组脊髓内基质金属蛋白酶2、9阳性细胞数少于模型对照组、自体嗅黏膜组、β-七叶皂甙钠组(P<0.05)。结果提示自体嗅黏膜移植与β-七叶皂甙钠之间有协同作用,可明显改善神经运动功能恢复情况;此种作用可能与其抑制基质金属蛋白酶2、9过度表达有关。

Effects of autologous olfactory mucoma combined with beta-aesine sodium on expression of matrix metalloproteinase-2 and matrix metalloproteinase-9 in rats following spinal cord injury

BACKGROUND:After spinal cord injury,over-expression of metalloproteinase-2(MMP-2) and matrix metalloproteinase-9(MMP-9) contributes to secondary tissue damage of the spinal cord.OJECTIVE:To study the influence of autologous olfactory mucoma combined with β-aesine sodium on expression of MMP-2,9 and the recovery of neural function of injured spinal cord in adult rats.METHODS:In this study,healthy Sprague-Dawley rats with T10 spinal cord hemisection were divided into four groups as follows:control group(A),autologous olfactory mucoma transplantation group(B),β-aesine sodium group(C),combination group(D).RESULTS AND CONCLUSION:The BBB scales showed that rats in groups B,C and D had more improvement than those in group A at series of phases at 7 and 14 days after operation(P < 0.05),and the BBB score of group D was much higher than that of group B and group C(P < 0.05).The expression of MMP-9 and MMP-2 in injured spinal cord increased significantly at all time points.The number of positive cells in group D was less than that in groups B and C at the corresponding time points(P < 0.05),but there were no statistically significant differences between group B and C(P > 0.05).The method of treating spinal cord injury by autologous olfactory mucosa transplantation combined with β-aesine sodium has good curative effect,and can largely improve hind limbs motor function,which may be related to inhibiting the overexpression of MMP-9 and MMP-2 genes.