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目的探讨缺氧缺血性脑损伤(HIBD)新生大鼠脑组织基质金属蛋白酶(MMPs)的动态变化及其与细胞凋亡的关系。方法将72只7日龄W istar大鼠随机分为假手术组和HIBD组,后者根据处死时间分为6 h、24 h、48 h、5天和14天组,每组12只。采用免疫组化方法测定MMP-2、MMP-9和金属蛋白酶组织抑制因子-1(TIMP-1)的表达,用流式细胞术测定脑细胞凋亡率。结果 HIBD组缺氧缺血侧大脑组织MMP-2于损伤6 h增高,5天再次升高,且峰值高于6 h组,与假手术组相比,除24 h组,其余差异均有统计学意义(P<0.05);MMP-9正常情况下有一定表达,HIBD 24 h表达达高峰,后逐渐下降,与假手术组相比,除14天组,差异均有统计学意义(P<0.05);TIMP-1正常情况下与MMP-9保持动态平衡,HIBD时两者比例失衡,后期表达增加两者平衡恢复,与假手术组相比,除6 h组和14天组,差异均有统计学意义(P<0.05)。HIBD组缺氧缺血侧脑细胞凋亡率24 h轻度升高,5天达高峰,与假手术组相比,除6 h组,差异均有统计学意义(P<0.05)。结论新生大鼠HIBD后MMP-2、MMP-9和TIMP-1的表达有不同程度变化,可能参与了HIBD的发病与修复。
Objective To investigate the dynamic changes of matrix metalloproteinases (MMPs) and its relationship with apoptosis in neonatal rats with hypoxic-ischemic brain damage (HIBD). Methods Seventy-two Wistar rats of 7 days old were randomly divided into sham operation group and HIBD group. The latter were divided into 6 h, 24 h, 48 h, 5 d and 14 d groups according to the sacrificial time, 12 in each group. The expression of MMP-2, MMP-9 and TIMP-1 were detected by immunohistochemistry. The apoptosis rate of brain cells was determined by flow cytometry. Results Compared with the sham group, the MMP-2 of HIBD group increased at 6 h, increased again at 5 d and peaked at 6 h (P <0.05). The expression of MMP-9 was normal in some cases. The expression of HIBD reached its peak at 24 h and then decreased gradually. Compared with the sham-operated group, except for the 14-day group, the difference was statistically significant (P < 0.05). Compared with the sham-operated group, the levels of TIMP-1 and MMP-9 remained homeostasis under normal conditions and the imbalance of HbD and the late stage of HIBD. There was statistical significance (P <0.05). Compared with the sham-operation group, the apoptosis rate of HIBD group increased slightly at 24 h and peaked at 5 d, except for 6 h group, the difference was statistically significant (P <0.05). Conclusions The expressions of MMP-2, MMP-9 and TIMP-1 in HIBD of newborn rats may have different degrees of change, which may be involved in the pathogenesis and repair of HIBD.