4.5 Article

Pathological changes of frozen shoulder in rat model and the therapeutic effect of PPAR-γ agonist

期刊

JOURNAL OF ORTHOPAEDIC RESEARCH
卷 39, 期 4, 页码 891-901

出版社

WILEY
DOI: 10.1002/jor.24920

关键词

animal model; frozen shoulder; PPAR‐ γ agonists

资金

  1. Shenzhen Double Chain Project [201806081524201510]
  2. National Natural Science Foundation of China [81672234, 81902303, 81902558]
  3. Shenzhen Science and Technology Project [GJHZ20180416164801042, JCYJ20180305124912336]
  4. Clinical Research Project of Shenzhen Second People's Hospital [20173357201814]

向作者/读者索取更多资源

The study investigated the effect of TGF-beta on frozen shoulder in rat models and explored the therapeutic effect of PPAR-gamma agonist. Results showed PPAR-gamma agonists may be a promising target for frozen shoulder treatment, reducing inflammation and abnormal cell proliferation.
Frozen shoulder is a common shoulder disorder characterized by a gradual increase of pain and a limited range of motion. However, its pathophysiologic mechanisms remain unclear and there is no consensus as to the most effective treatment. The purpose of the study was to investigate the effect of transforming growth factor-beta (TGF-beta) on fibrosis and inflammatory response of the shoulder joint of rat models and to explore the therapeutic effect of the peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist. In the study, the effect of PPAR-gamma agonist CDDO-IM treatment on cell proliferation, migration, and extracellular matrix proteins synthesis (vimentin, alpha-smooth muscle actin, collagen I, and collagen III) were tested by cell proliferation test, scratches test, real-time quantitative polymerase chain reaction, and Western blot analysis. The frozen shoulder was also established on the rat model by injecting adenovirus-TGF-beta 1 into rats' shoulder capsule. Pathological changes of the frozen shoulder tissue of the experimental group and PPAR-gamma agonist treatment group were evaluated. The stiffness of joints of the three groups was tested. Inflammatory mediators' expression including cyclooxygenase-1, interleukin-1 beta, and tumor necrosis factor-alpha of the shoulder was tested by enzyme-linked immunosorbent assay, and the expression of extracellular matrix proteins was evaluated by hematoxylin and eosin staining and immunohistochemistry. The results showed that pathological changes of the frozen shoulder in the rat model include an abnormal proliferation of fibroblasts, infiltration of inflammatory cells, and disorder of fibrous structure, while rosiglitazone reduced the severity of the frozen shoulder in the treatment group. Clinically, PPAR-gamma agonists may be a promising target for the treatment of the frozen shoulder.

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