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p38 丝裂原活化蛋白激酶抑制物下调钛颗粒诱导的小鼠骨溶解模型中的炎症性骨溶解反应。

Inhibition of p38 mitogen-activated protein kinase down-regulates the inflammatory osteolysis response to titanium particles in a murine osteolysis model.

机构信息

Department of Orthopaedics, The Sixth Affiliated People's Hospital, School of Medicine, Shanghai Jiao Tong University, No. 600 Yishan Road, Shanghai 200233, China.

出版信息

Inflammation. 2012 Dec;35(6):1798-806. doi: 10.1007/s10753-012-9500-3.

Abstract

The p38 mitogen-activated protein kinase (p38 MAPK) pathway is involved in the osteoclast differentiation. The aim of the study was to investigate whether SB203580, a p38 MAPK inhibitor, inhibits wear-debris-induced inflammatory osteolysis in mice. Forty-five mice were implanted with calvaria bone from syngeneic littermates; then, titanium (Ti) particles were injected into established air pouches to provoke inflammatory osteolysis. At 14 days after bone/Ti implantation, pouch membranes with intact bone implants underwent histological and molecular analysis. SB203580 had less effect on MMP-9 and TNF-α expression under wear-debris-induced conditions. SB203580, by inhibiting the expression of p38 MAPK and phospho-p38 MAPK, inhibited Ti particle wear-debris-induced inflammatory osteolysis. It also remarkably decreased the number of tartrate-resistant acid phosphatase positive cells in Ti-particle-induced pouch tissues. Results suggest that p38 MAPK may be critical in a murine osteolysis model. SB203580 may notably inhibit wear-debris-induced inflammatory osteolysis by down-regulating expression of MMP-9 and TNF-α via the p38 MAPK pathway.

摘要

p38 丝裂原活化蛋白激酶(p38 MAPK)途径参与破骨细胞分化。本研究旨在探讨 p38 MAPK 抑制剂 SB203580 是否抑制小鼠磨损颗粒诱导的炎症性骨溶解。将 45 只小鼠植入同基因同窝仔鼠的颅骨;然后,将钛(Ti)颗粒注入已建立的气囊中以引发炎症性骨溶解。在骨/Ti 植入后 14 天,对完整骨植入物的囊膜进行组织学和分子分析。在磨损颗粒诱导的条件下,SB203580 对 MMP-9 和 TNF-α表达的影响较小。SB203580 通过抑制 p38 MAPK 和磷酸化 p38 MAPK 的表达,抑制了 Ti 颗粒磨损颗粒诱导的炎症性骨溶解。它还显著减少了 Ti 颗粒诱导的囊组织中抗酒石酸酸性磷酸酶阳性细胞的数量。结果表明,p38 MAPK 在小鼠骨溶解模型中可能是关键的。SB203580 通过 p38 MAPK 途径下调 MMP-9 和 TNF-α 的表达,显著抑制磨损颗粒诱导的炎症性骨溶解。

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