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首页> 外文期刊>Digestive Diseases and Sciences >Rat Gastric Gelatinase Induction During Endotoxemia
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Rat Gastric Gelatinase Induction During Endotoxemia

机译：内毒素血症期间大鼠胃明胶酶的诱导

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Despite continued investigation, the pathogenesis of tissue injury secondary to sepsis remains elusive. Further evaluation of the mechanisms by which endotoxemia and sepsis induce tissue injury is necessary to formulate rational and effective treatment strategies. The purpose of these studies was to evaluate the role of the matrix metalloproteinases MMP-2 and MMP-9 in gastric injury during lipopolysaccharide induced endotoxemia. Lipopolysaccharide increased gastric gelatinase activity as determined by in situ and gelatin zymography. Specifically, lipopolysaccharide induced MMP-2, MMP-9, and tissue inhibitor of metalloproteinase-1 (TIMP-1) transcription, with subsequent increases in MMP-2 and TIMP-1 protein expression. Furthermore, selective metalloproteinase inhibition ameliorated gastric injury in this model. These data suggest that lipopolysaccharide-induced gastric injury is mediated, at least in part, by increased MMP-2 production.
机译：尽管进行了持续的研究，败血症继发的组织损伤的发病机制仍然难以捉摸。为了制定合理和有效的治疗策略，有必要进一步评估内毒素血症和败血症诱导组织损伤的机制。这些研究的目的是评估基质金属蛋白酶MMP-2和MMP-9在脂多糖诱导的内毒素血症期间对胃损伤的作用。通过原位和明胶酶谱测定，脂多糖增加了胃明胶酶活性。具体而言，脂多糖诱导MMP-2，MMP-9和金属蛋白酶-1（TIMP-1）的组织抑制剂，随后MMP-2和TIMP-1蛋白表达增加。此外，在该模型中，选择性金属蛋白酶抑制改善了胃损伤。这些数据表明，脂多糖诱导的胃损伤至少部分地由增加的MMP-2产生介导。

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