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首页> 外文期刊>Journal of orthopaedic research >Low-intensity pulsed ultrasound protects subchondral bone in rabbit temporomandibular joint osteoarthritis by suppressing TGF-beta 1/Smad3 pathway
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Low-intensity pulsed ultrasound protects subchondral bone in rabbit temporomandibular joint osteoarthritis by suppressing TGF-beta 1/Smad3 pathway

机译:低强度脉冲超声通过抑制TGF-β1/ Smad3途径来保护兔颞下颌关节骨关节炎中的子骨髓骨骼

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摘要

Transforming growth factor beta 1(TGF-beta 1)/Smad3 pathway promotes the pathological progression of subchondral bone in osteoarthritis. The aim of this study is to determine the effect of low-intensity pulsed ultrasound (LIPUS) on the pathological progression and TGF-beta 1/Smad3 pathway of subchondral bone in temporomandibular joint osteoarthritis (TMJOA). Rabbit TMJOA model was established by type II collagenase induction. The left joint in this model was continuously stimulated with LIPUS for 3 and 6 weeks (1 MHz; 30 mW/cm(2)) for 20 min/day. The morphological and histological features of subchondral bone were respectively examined by microcomputed tomography and Safranin-O staining. The number of osteoclasts was quantitatively assessed by tartrate-resistant acid phosphatase staining. Immunohistochemistry and Western blot analysis were conducted to evaluate the protein expression of Cathepsin K and TGF-beta 1/Smad3 pathway. The results indicated that LIPUS could improve the trabecular microstructure and histological characteristics of subchondral bone in rabbit TMJOA. It also suppressed abnormal subchondral bone resorption and activation of TGF-beta 1/Smad3 pathway, characterized by the number of osteoclasts, protein expression levels of Cathepsin K, TGF-beta 1, type II TGF beta receptor, and phosphorylated Smad3 (pSmad3) were decreased. In conclusion, LIPUS promoted the quality of subchondral bone by suppressing osteoclast activity and TGF-beta 1/Smad3 pathway in rabbit TMJOA.
机译:转化生长因子β1(TGFβ1)/Smad3途径促进骨关节炎软骨下骨的病理进展。本研究的目的是确定低强度脉冲超声(LIPUS)对颞下颌关节骨关节炎(TMJOA)软骨下骨的病理进展和TGF-β1/Smad3通路的影响。通过II型胶原酶诱导建立兔TMJOA模型。在这个模型中,用LIPUS连续刺激左关节3周和6周(1 MHz;30 mW/cm(2))20分钟/天。采用显微计算机断层扫描和藏红O染色分别观察软骨下骨的形态和组织学特征。抗酒石酸酸性磷酸酶染色定量测定破骨细胞数量。免疫组织化学和Western blot分析评估组织蛋白酶K和TGF-β1/Smad3通路的蛋白表达。结果表明,LIPUS可以改善兔TMJOA软骨下骨的小梁显微结构和组织学特征。它还抑制了异常的软骨下骨吸收和TGF-β1/Smad3途径的激活,其特征是破骨细胞的数量、组织蛋白酶K、TGF-β1、II型TGF-β受体和磷酸化Smad3(pSmad3)的蛋白表达水平降低。总之,LIPUS通过抑制兔TMJOA中的破骨细胞活性和TGF-β1/Smad3途径,提高了软骨下骨的质量。

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