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首页> 外文期刊>Journal of applied toxicology >Effects of acetyl salycilic acid and ibuprofen in chronic liver damage induced by CCI_4
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Effects of acetyl salycilic acid and ibuprofen in chronic liver damage induced by CCI_4

机译：乙酰水杨酸和布洛芬对CCL4诱导的慢性肝损伤的作用

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ABSTRACT: Non-steroidal anti-inflammatory drugs (NSAIDs) are drugs used primarily to treat inflammation, pain and fever. Their main mechanism of action is cyclooxygenase (COX) inhibition, and this enzyme has been linked to hepatotoxicity. The association of COX and liver injury has been, in part, due to the presence of COX-2 isoform in damaged liver and the possible induction of this enzyme by profibrotic molecules like Transforming Growth Factor-beta (TGF-beta). The aim of this work was to evaluate the effects of two of the most used NSAIDs, acetyl salicylic acid (ASA) and ibuprofen (IBP), on experimental liver fibrosis. We formed experimental groups of rats including vehicle and drug controls, damage induced by chronic CCI4 (0.4 g kg~(-1), i.p., three times per week, for 8 weeks) administration, and CCI_4 plus ASA (100 mg kg~(-1), p.o., daily) or IBP (30 mg kg~(-1), p.o., daily). Both drugs showed important antifibrotic properties. They inhibited COX-2 activity, prevented oxidative stress measured as lipid peroxidation and glutathione content, and ASA inhibited partially and IBP totally increased TGF-/3 expression and collagen content. ASA and IBP prevented translocation of NFkappaB to the nucleus and, interestingly, ASA induced MMP-2 and MMP-13 whereas IBP induced MMP-2, MMP-9 and MMP-13. As a whole, these effects explain the beneficial effects of ASA and IBP on experimental liver fibrosis.
机译：摘要：非甾体类抗炎药（NSAIDs）是主要用于治疗炎症，疼痛和发烧的药物。它们的主要作用机理是抑制环氧合酶（COX），并且该酶与肝毒性有关。 COX与肝损伤的关系部分是由于受损肝中存在COX-2同工型，以及诸如转化生长因子-β（TGF-beta）等纤维化分子可能对该酶的诱导。这项工作的目的是评估两种最常用的NSAID（乙酰水杨酸（ASA）和布洛芬（IBP））对实验性肝纤维化的影响。我们形成了实验组的大鼠，包括赋形剂和药物对照，慢性CCI4（0.4 g kg〜（-1），腹腔注射，每周三次，连续8周）和CCI_4加ASA（100 mg kg〜（ -1），每天一次）或IBP（30 mg kg〜（-1），每天一次）。两种药物均显示出重要的抗纤维化特性。它们抑制COX-2活性，防止氧化应激（以脂质过氧化和谷胱甘肽含量衡量），而ASA则部分抑制，IBP完全增加TGF- / 3表达和胶原蛋白含量。 ASA和IBP阻止NFkappaB转运到细胞核，有趣的是，ASA诱导MMP-2和MMP-13，而IBP诱导MMP-2，MMP-9和MMP-13。总体而言，这些作用解释了ASA和IBP对实验性肝纤维化的有益作用。

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