Life Sci. 2013 Dec 18;93(25-26):1033-8.
To evaluate the effects of hyperbaric oxygen (HBO) therapy on MMP-2 and MMP-9 expression and spinal cord edema after acute spinal cord injury (SCI).
Ninety-six healthy adult Sprague − Dawley rats were randomly divided into 4 groups: sham, sham + HBO, SCI, and SCI + HBO. Each group was subdivided into 4 subgroups of 6 rats each: 24 h, 48 h, 72 h, and 5 d post-injury. The expression levels of matrix metalloproteinase-2 (MMP-2), MMP-9, interleukin (IL-6), and vascular endothelial growth factor (VEGF) were measured using ELISA. The water content of the spinal cord was also measured by Elliot equation.
MMP-2 and MMP-9 levels and spinal cord water content increased significantly in the SCI group compared to those in the sham and sham + HBO groups at different time points after SCI (P < 0.01). The MMP-2 level was significantly different between the SCI and SCI + HBO groups at 72 h after SCI (P < 0.05), while the MMP-9 level was significantly different at 48 h, 72 h, and 5 d (P < 0.05). The water content of the spinal cord was significantly higher in the SCI group at 5 d after SCI (P < 0. 01). MMP-2 (P < 0.05) and MMP-9 (P < 0.01) levels were positively correlated with spinal cord water content.
HBO reduced SCI-induced spinal cord edema, stabilized the blood-spinal cord barrier, and promoted recovery of neuronal function by down regulating the expression of IL-6, MMP-2, and MMP-9 and up regulating the expression of VEGF.
评估高压氧(HBO)治疗对急性脊髓损伤(SCI)后 MMP-2 和 MMP-9 表达及脊髓水肿的影响。
96 只健康成年 Sprague-Dawley 大鼠随机分为 4 组:假手术组、假手术+HBO 组、SCI 组和 SCI+HBO 组。每组再分为 4 个亚组,每组 6 只大鼠,分别于损伤后 24 h、48 h、72 h 和 5 d。采用 ELISA 法检测基质金属蛋白酶-2(MMP-2)、MMP-9、白细胞介素(IL-6)和血管内皮生长因子(VEGF)的表达水平。采用 Elliot 方程测量脊髓含水量。
与假手术组和假手术+HBO 组相比,SCI 组在 SCI 后不同时间点 MMP-2 和 MMP-9 水平及脊髓含水量均显著升高(P<0.01)。SCI 后 72 h,SCI 组和 SCI+HBO 组 MMP-2 水平差异有统计学意义(P<0.05),而 MMP-9 水平在 48 h、72 h 和 5 d 时差异有统计学意义(P<0.05)。SCI 后 5 d,SCI 组脊髓含水量明显升高(P<0.01)。MMP-2(P<0.05)和 MMP-9(P<0.01)水平与脊髓含水量呈正相关。
HBO 通过下调 IL-6、MMP-2 和 MMP-9 的表达及上调 VEGF 的表达,减轻 SCI 引起的脊髓水肿,稳定血脊髓屏障,促进神经元功能恢复。