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【bio-news】脊髓损伤后MMP2/MMP9抑制减少凋亡。
Spine. 33(17):E576-E579, August 1, 2008.
Study Design. Randomized controlled trial.
Objective. To characterize the increase in gelatinase A (MMP2) activity after spinal cord injury (SCI) in the mouse model, and the effects of MMP2/MMP9 inhibition on apoptotic cells.
Summary of Background Data. Clinical consequences of SCI are due to a series of secondary injury cascades. Matrix metalloproteinases are thought play a key role in this, leading to apoptotic cell death.
Methods. SCI via a drop tower in mice was used. MMP2 [beta]-gal reporter mice were used to quantify the level of MMP2 after SCI. In a follow-up experiment, mice which underwent SCI were randomized to daily SQ injections of MMP2/MMP9 inhibitor versus placebo. MMP2 levels were quantified and histology was performed with TUNEL and Luxol fast blue staining.
Results. MMP2 transcription was significantly upregulated after SCI, by the [beta]-gal assay. Inhibition of MMP2/MMP9 activity after SCI led to statistically significant decreases in apoptosis within the zone of injury. There was a trend towards preservation of myelin by preserved luxol fast blue staining.
Conclusion. After SCI, MMP2 is upregulated along with neuron and glial cells apoptosis. The level of apoptosis could be reduced with MMP2/MMP9 inhibition. This supports MMP2 as cause for apoptosis after SCI with the potential for therapeutic intervention as apoptosis can be reduced with MMP2 inhibition.
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本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领 Inhibition of MMP2/MMP9 After Spinal Cord Trauma Reduces Apoptosis.
Spine. 33(17):E576-E579, August 1, 2008.
脊髓损伤后MMP2/MMP9抑制减少凋亡。
Abstract: 摘要
Study Design. Randomized controlled trial.
研究设计 随机对照研究
Objective. To characterize the increase in gelatinase A (MMP2) activity after spinal cord injury (SCI) in the mouse model, and the effects of MMP2/MMP9 inhibition on apoptotic cells.
目的 在小鼠动物模型中，明确脊髓损伤后明胶酶A (MMP2)活性增加，以及MMP2/MMP9抑制导致细胞凋亡的影响。
Summary of Background Data. Clinical consequences of SCI are due to a series of secondary injury cascades. Matrix metalloproteinases are thought play a key role in this, leading to apoptotic cell death.
背景知识概述 SCI的临床结果是由于一系列继发性损伤级联反应造成的。MMP被认为是在这过程起了关键性作用，导致了凋亡性细胞死亡。
Methods. SCI via a drop tower in mice was used. MMP2 [beta]-gal reporter mice were used to quantify the level of MMP2 after SCI. In a follow-up experiment, mice which underwent SCI were randomized to daily SQ injections of MMP2/MMP9 inhibitor versus placebo. MMP2 levels were quantified and histology was performed with TUNEL and Luxol fast blue staining.
方法 通过落塔的方法用于小鼠的SCI造模。MMP2-[beta]半乳糖报告小鼠用于定量分析SCI后MMP2的水平。在随后的实验中，SCI小鼠被随机分为MMP2/MMP9抑制剂注射组和安慰剂组。MMP2水平定量分析，采用TUNEL方法和LuxolFastBlue染色技术做组织学分析。
Results. MMP2 transcription was significantly upregulated after SCI, by the [beta]-gal assay. Inhibition of MMP2/MMP9 activity after SCI led to statistically significant decreases in apoptosis within the zone of injury. There was a trend towards preservation of myelin by preserved luxol fast blue staining.
结果 通过[beta]半乳糖检测，SCI后MMP2转录明显上调。SCI后MMP2/MMP9活性的抑制导致损伤区域凋亡明显的下降。LuxolFastBlue染色技术表明存在髓鞘保留的趋势。
Conclusion. After SCI, MMP2 is upregulated along with neuron and glial cells apoptosis. The level of apoptosis could be reduced with MMP2/MMP9 inhibition. This supports MMP2 as cause for apoptosis after SCI with the potential for therapeutic intervention as apoptosis can be reduced with MMP2 inhibition.
结论 在SCI后，MMP2的上调与神经元和神经胶质细胞凋亡一致。凋亡的水平可以被MMP2/MMP9抑制剂减少。这就支持MMP2是SCI后凋亡的因素之一，抑制MMP2来减少凋亡有可能作为治疗干预方法。 编译：
脊髓损伤后MMP2/MMP9抑制减少凋亡。
在小鼠动物模型中，明确脊髓损伤后明胶酶A (MMP2)活性增加，以及MMP2/MMP9抑制导致细胞凋亡的影响。SCI的临床结果是由于一系列继发性损伤级联反应造成的。MMP被认为是在这过程起了关键性作用，导致了凋亡性细胞死亡。 通过落塔的方法用于小鼠的SCI造模。MMP2-[beta]半乳糖报告小鼠用于定量分析SCI后MMP2的水平。在随后的实验中，SCI小鼠被随机分为MMP2/MMP9抑制剂注射组和安慰剂组。MMP2水平定量分析，采用TUNEL方法和LuxolFastBlue染色技术做组织学分析。通过[beta]半乳糖检测，SCI后MMP2转录明显上调。SCI后MMP2/MMP9活性的抑制导致损伤区域凋亡明显的下降。LuxolFastBlue染色技术表明存在髓鞘保留的趋势。在SCI后，MMP2的上调与神经元和神经胶质细胞凋亡一致。凋亡的水平可以被MMP2/MMP9抑制剂减少。这就支持MMP2是SCI后凋亡的因素之一，抑制MMP2来减少凋亡有可能作为治疗干预方法。 spine journal, it is difficult for me to say loving you!
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作者:admin@医学,生命科学 2010-11-07 17:11
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