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白细胞介素-1α诱导牛关节软骨中与胶原蛋白降解相关的拉伸弱化。

Interleukin-1alpha induction of tensile weakening associated with collagen degradation in bovine articular cartilage.

作者信息

Temple Michele M, Xue Yang, Chen Michael Q, Sah Robert L

机构信息

University of California, San Diego, CA 92093-0412, USA.

出版信息

Arthritis Rheum. 2006 Oct;54(10):3267-76. doi: 10.1002/art.22145.

Abstract

OBJECTIVE

To determine whether interleukin-1alpha (IL-1alpha) induces tensile weakening of articular cartilage that is concomitant with the loss of glycosaminoglycans (GAGs) or the subsequent degradation of the collagen network.

METHODS

Explants of young adult bovine cartilage obtained from the superficial (including the articular surface), middle, and deep layers were cultured with or without IL-1alpha for 1 week or 3 weeks. Then, portions of the explants were analyzed for their tensile properties (ramp modulus, strength, and failure strain); other portions of explants and spent culture medium were analyzed for the amount of GAG and the amount of cleaved, denatured, and total collagen.

RESULTS

The effect of IL-1alpha treatment on cartilage tensile properties and content was dependent on the duration of culture and the depth of the explant from the articular surface. The tensile strength and failure strain of IL-1alpha-treated samples from the superficial and middle layers were lower after 3 weeks of culture, but not after 1 week of culture. However, by 1 week of culture, IL-1alpha had already induced release of the majority of tissue GAGs into the medium, without detectable loss or degradation of collagen. In contrast, after 3 weeks of culture, IL-1alpha induced significant collagen degradation, as indicated by the amount of total, cleaved, or denatured collagen in the medium or in explants from the superficial and middle layers.

CONCLUSION

IL-1alpha-induced degradation of cartilage results in tensile weakening that occurs subsequent to the depletion of GAG and concomitant with the degradation of the collagen network.

摘要

目的

确定白细胞介素-1α(IL-1α)是否会诱导关节软骨拉伸强度减弱,这一过程是否与糖胺聚糖(GAGs)的丢失或随后胶原网络的降解相关。

方法

从幼年成年牛软骨的表层(包括关节表面)、中层和深层获取外植体,分别在有或无IL-1α的条件下培养1周或3周。然后,分析部分外植体的拉伸性能(斜坡模量、强度和断裂应变);分析外植体的其他部分以及用过的培养基中GAG的含量、裂解、变性和总胶原的含量。

结果

IL-1α处理对软骨拉伸性能和含量的影响取决于培养时间和外植体距关节表面的深度。培养3周后,表层和中层经IL-1α处理的样本的拉伸强度和断裂应变降低,但培养1周后未出现这种情况。然而,培养1周时,IL-1α已诱导大部分组织GAG释放到培养基中,而胶原未出现可检测到的丢失或降解。相比之下,培养3周后,IL-1α诱导了显著的胶原降解,这可通过培养基中或表层和中层外植体中的总胶原、裂解胶原或变性胶原的含量来表明。

结论

IL-1α诱导的软骨降解导致拉伸强度减弱,这发生在GAG耗竭之后,并与胶原网络的降解同时出现。

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