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首页> 外文期刊>Molecular medicine reports >Visceral adipose tissue-derived serine protease inhibitor inhibits interleukin-1β-induced catabolic and inflammatory responses in murine chondrocytes.
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Visceral adipose tissue-derived serine protease inhibitor inhibits interleukin-1β-induced catabolic and inflammatory responses in murine chondrocytes.

机译:内脏脂肪组织衍生的丝氨酸蛋白酶抑制剂可抑制白细胞介素1β诱导的小鼠软骨细胞分解代谢和炎症反应。

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摘要

Visceral adipose tissue-derived serine protease inhibitor (vaspin) is a newly identified member of the adipocytokine family, whose precise role in chondrocyte metabolism remains to be elucidated. The aim of the present study was to investigate the effect of vaspin on chondrocytes. The cell viability and the cytotoxicity of vaspin in chondrocytes were examined. Furthermore, the gene expression of matrix metalloproteinases-2 and -9, a disintegrin and metalloproteinase with thrombospondin motifs 4 and 5 and cathepsin D was also examined, as well as the protein production of cyclooxygenase-2, prostaglandin E2 and inducible nitrous oxide synthase following treatment with different concentrations of vaspin in the absence or presence of interleukin-1-beta (IL-1β). In addition, the protein levels of the inhibitor of nuclear factor-κB (IκB-α) and the phosphorylation of nuclear factor kappa B (NF?κB) were investigated. Vaspin was not able to stimulate the proliferation of chondrocytes and demonstrated no significant cytotoxic effect at concentrations of 10-500 ng/ml following coincubation for 24 and 48 h. However, vaspin inhibited IL-1β?induced production of catabolic factors and inflammatory mediators in chondrocytes, and also suppressed the phosphorylation of NF?κB and the degradation of IκB?α. The data from the present study suggested that vaspin has a protective effect in chondrocyte metabolism and is an important factor in the pathophysiology of osteoarthritis.
机译:内脏脂肪组织衍生的丝氨酸蛋白酶抑制剂(vaspin)是脂肪细胞因子家族的新成员,其在软骨细胞代谢中的确切作用尚待阐明。本研究的目的是研究vaspin对软骨细胞的影响。检查了vaspin在软骨细胞中的细胞活力和细胞毒性。此外,还检查了基质金属蛋白酶-2和-9,具有血小板反应蛋白基序4和5以及组织蛋白酶D的解整合素和金属蛋白酶的基因表达,以及随后的环氧合酶-2,前列腺素E2和诱导型一氧化二氮合酶的蛋白产生。在不存在或存在白介素-1-β(IL-1β)的情况下,用不同浓度的vaspin进行治疗。此外,还研究了核因子-κB(IκB-α)抑制剂的蛋白水平和核因子-κB(NF?κB)的磷酸化。共孵育24和48小时后,Vaspin不能刺激软骨细胞的增殖,并且在10-500 ng / ml的浓度下没有表现出明显的细胞毒性作用。但是,vaspin抑制IL-1β诱导的软骨细胞中分解代谢因子和炎性介质的产生,并抑制NFκB的磷酸化和IκBα的降解。来自本研究的数据表明,vaspin对软骨细胞代谢具有保护作用,并且是骨关节炎病理生理学的重要因素。

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