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首页> 外文期刊>International journal of molecular medicine >Tougu Xiaotong capsule inhibits the tidemark replication and cartilage degradation of papain-induced osteoarthritis by the regulation of chondrocyte autophagy
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Tougu Xiaotong capsule inhibits the tidemark replication and cartilage degradation of papain-induced osteoarthritis by the regulation of chondrocyte autophagy

机译：头骨消痛胶囊通过调节软骨细胞自噬，抑制木瓜蛋白酶诱导的骨关节炎的潮汐复制和软骨降解

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摘要

The tidemark is located between calcified and non-calcified cartilage matrices. Tidemark replication plays an important role in the pathogenesis of osteoarthrosis (OA). Autophagy, or cellular self-digestion, is an essential cellular homeostasis mechanism that was found to be deficient in osteoarthritic cartilage. This study evaluated the effects of Tougu Xiaotong capsule (TXC) on the tidemark replication and cartilage degradation, and also investigated LC3 I/II, which executes autophagy, the potential role of ULK1, an inducer of autophagy, and Beclin1, a regulator of autophagy, in the development of a papain-induced OA in rat knee joints. Using a papain-injected knee rat model, standard histological methods were used to validate our model as well as treatment with TXC or glucosamine (GlcN). After 12 weeks of treatment, the changes of cartilage structure were observed by digital radiography (DR), optical microscopy, scanning electron microscopy and transmission electron microscopy, and the LC3 I/II, ULK1 and Beclin1 levels were measured by western blotting. Cartilage degradation was evaluated by the Mankin score on paraffin-embedded sections stained with Safranin O-fast green. TXC was found to improve the arrangement of subchondral bone collagen fi bers and calcium phosphate crystals, inhibit the tidemark replication and delay the cartilage degradation in the papain-induced OA. Our results also showed that LC3 I/II, ULK1 and Beclin1 levels in both the TXC+OA and GlcN+OA groups were signifi cantly increased compared to those in the OA group. The results indicate that TXC could inhibit the tidemark replication and cartilage degradation by the regulation of chondrocyte autophagy.
机译：潮标位于钙化和非钙化的软骨基质之间。 Tidemark复制在骨关节炎（OA）的发病机理中起着重要作用。自噬或细胞自我消化是一种基本的细胞体内稳态机制，被发现在骨关节炎软骨中缺乏。这项研究评估了头固消痛胶囊（TXC）对潮标复制和软骨降解的影响，并研究了执行自噬的LC3 I / II，自噬诱导剂ULK1和自噬调节剂Beclin1的潜在作用。 ，在木瓜蛋白酶诱导的大鼠膝关节骨关节炎的发展中。使用木瓜蛋白酶注射的膝盖大鼠模型，使用标准的组织学方法来验证我们的模型以及TXC或葡萄糖胺（GlcN）的治疗。治疗12周后，通过数字射线照相术（DR），光学显微镜，扫描电子显微镜和透射电子显微镜观察软骨结构的变化，并通过蛋白质印迹法测量LC3 I / II，ULK1和Beclin1水平。通过Mankin评分对用番红O型至坚牢绿色染色的石蜡包埋切片评估软骨降解。发现TXC改善了软骨下骨胶原纤维和磷酸钙晶体的排列，抑制了潮标复制并延迟了木瓜蛋白酶诱导的OA中的软骨降解。我们的结果还表明，与OA组相比，TXC + OA和GlcN + OA组中的LC3 I / II，ULK1和Beclin1水平均显着增加。结果表明，TXC可通过调节软骨细胞自噬来抑制潮汐标记复制和软骨降解。

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