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Tetrahydrohyperforin prevents articular cartilage degeneration and affects autophagy in rats with osteoarthritis

机译:Tetrahydrohyperforin可预防骨关节炎大鼠的关节软骨变性并影响自噬

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摘要

Osteoarthritis (OA) is a highly prevalent disease, which is associated with extracellular matrix degradation and cell death in articular cartilage. The aim of the present study was to identify whether tetrahydrohyperforin (IDN5706) ameliorates the degeneration of articular cartilage and affects autophagy in OA. The rat model of experimental OA was induced by intra-articular injection of collagenase solution. IDN5706 was administered intragastrically to rats for 6 weeks. Histopathological changes in articular cartilage were examined using hematoxylin and eosin (H&E) and safranin O staining, and Mankin scoring systems. The effect of IDN5706 on autophagy was examined using western blotting. ELISA was performed to detect cartilage inflammation. H&E and safranin O staining, Mankin scores, and electron microscopy indicated that IDN5706 could lessen the degeneration of articular cartilage in OA rats. In addition, western blotting revealed that IDN5706 treatment may activate the suppressed autophagy in OA rats. In conclusion, the present study demonstrated that IDN5706 was able to reduce the severity of experimental OA, alleviate the degeneration of articular cartilage, and affect autophagy in OA model rats.
机译:骨关节炎(OA)是一种高度流行的疾病,与关节软骨中的细胞外基质降解和细胞死亡有关。本研究的目的是确定四氢高蛋白(IDN5706)是否可改善关节软骨的变性并影响OA中的自噬。通过关节内注射胶原酶溶液诱导大鼠实验性OA模型。将IDN5706灌胃给予大鼠6周。使用苏木精和曙红(H&E)和番红蛋白O染色以及Mankin评分系统检查关节软骨的组织病理学变化。使用蛋白质印迹检查了IDN5706对自噬的影响。进行ELISA以检测软骨炎症。 H&E和番红O染色,Mankin评分和电子显微镜检查表明IDN5706可以减轻OA大鼠关节软骨的变性。此外,蛋白质印迹显示IDN5706处理可能会激活OA大鼠中抑制的自噬。总之,本研究证明IDN5706能够减轻实验性OA的严重性,减轻关节软骨的变性并影响OA模型大鼠的自噬。

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