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芝麻素的软骨保护和抗炎作用。

Chondroprotective and anti-inflammatory effects of sesamin.

机构信息

Thailand Excellence Center for Tissue Engineering and Stem Cells, Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.

出版信息

Phytochemistry. 2012 Aug;80:77-88. doi: 10.1016/j.phytochem.2012.05.016. Epub 2012 Jun 14.

DOI:10.1016/j.phytochem.2012.05.016
PMID:22704650
Abstract

Osteoarthritis (OA) is a major disability of elderly people. Sesamin is the main compound in Sesamun indicum Linn., and it has an anti-inflammatory effect by specifically inhibiting Δ5-desaturase in polyunsaturated fatty acid biosynthesis. The chondroprotective effects of sesamin were thus studied in a porcine cartilage explant induced with interleukin-1beta (IL-1β) and in a papain-induced osteoarthritis rat model. With the porcine cartilage explant, IL-1β induced release of sulfated-glycosaminoglycan (s-GAG) and hydroxyproline release, and this induction was significantly inhibited by sesamin. This ability to inhibit these processes might be due to its ability to decrease expression of MMP-1, -3 and -13, which can degrade both PGs and type II collagen, both at the mRNA and protein levels. Interestingly, activation of MMP-3 might also be inhibited by sesamin. Moreover, in human articular chondrocytes (HACs), some pathways of IL-1β signal transduction were inhibited by sesamin: p38 and JNK. In the papain-induced OA rat model, sesamin treatment reversed the following pathological changes in OA cartilage: reduced disorganization of chondrocytes in cartilage, increased cartilage thickness, and decreased type II collagen and PGs loss. Sesamin alone might increase formation of type II collagen and PGs in the cartilage tissue of control rats. These results demonstrate that sesamin efficiently suppressed the pathological processes in an OA model. Thus, sesamin could be a potential therapeutic strategy for treatment of OA.

摘要

骨关节炎(OA)是老年人的主要残疾。芝麻素是芝麻中的主要化合物,它通过特异性抑制多不饱和脂肪酸生物合成中的Δ5-脱饱和酶具有抗炎作用。因此,研究了芝麻素对白细胞介素-1β(IL-1β)诱导的猪软骨外植体和木瓜蛋白酶诱导的骨关节炎大鼠模型中的软骨保护作用。在猪软骨外植体中,IL-1β诱导硫酸化糖胺聚糖(s-GAG)和羟脯氨酸释放,芝麻素可显著抑制这种诱导作用。这种抑制这些过程的能力可能是由于其降低 MMP-1、-3 和 -13 的表达的能力,这些酶可以降解 PG 和 II 型胶原,在 mRNA 和蛋白质水平上都是如此。有趣的是,芝麻素也可以抑制 MMP-3 的激活。此外,在人关节软骨细胞(HAC)中,芝麻素抑制了 IL-1β信号转导的某些途径:p38 和 JNK。在木瓜蛋白酶诱导的 OA 大鼠模型中,芝麻素治疗逆转了 OA 软骨中的以下病理变化:软骨细胞在软骨中的排列紊乱减少,软骨厚度增加,以及 II 型胶原和 PGs 减少。芝麻素本身可能会增加对照组大鼠软骨组织中 II 型胶原和 PGs 的形成。这些结果表明芝麻素能有效抑制 OA 模型中的病理过程。因此,芝麻素可能是治疗 OA 的一种潜在治疗策略。

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