Berberine ameliorates cartilage degeneration in interleukin-1β-stimulated rat chondrocytes and in a rat model of osteoarthritis via Akt signalling
Berberine ameliorates cartilage degeneration in interleukin-1β-stimulated rat chondrocytes and in a rat model of osteoarthritis via Akt signalling
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小檗碱通过 Akt 信号传导改善白细胞介素 1 β 刺激的大鼠软骨细胞和骨关节炎大鼠模型中的软骨退变
DOI：
10.1111/jcmm.12186
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发表时间：
2014-02-01
影响因子：
5.3
通讯作者：
Zhang, Bing
中科院分区：
文献类型：
--
作者：
Zhao, Honghai;Zhang, Tongen;Zhang, Bing
小檗碱是一种用于中药的植物生物碱，在多种细胞系中具有广泛的细胞保护作用。软骨细胞凋亡参与骨关节炎（OA）软骨退变的发病机制。然而，小檗碱对骨性关节炎软骨细胞的作用及其机制尚不清楚。在这里，我们评估了小檗碱对白细胞介素-1 （IL-1）刺激的大鼠软骨细胞和OA大鼠模型中软骨变性的影响。MTT和western blotting结果显示，小檗碱能减弱IL-1对大鼠软骨细胞活力和增殖细胞核抗原表达的抑制作用。此外，小檗碱激活Akt，触发p70S6K/S6通路，上调il -1刺激的大鼠软骨细胞中aggrecan和Col II的表达水平。此外，通过组织病理学和免疫组织化学技术证实，小檗碱增加软骨基质中蛋白聚糖的水平和关节软骨的厚度，并提高大鼠OA模型中Col II、p-Akt和p-S6的表达水平。因此，这些数据强烈表明，小檗碱可能通过促进细胞存活和软骨细胞的基质生成来改善OA软骨变性，这在一定程度上归因于Akt在il -1刺激的关节软骨细胞和大鼠OA模型中的激活。由此产生的软骨保护作用表明，小檗碱值得考虑作为OA的治疗剂。
Berberine, a plant alkaloid used in Chinese medicine, has broad cell-protective functions in a variety of cell lines. Chondrocyte apoptosis contributes to the pathogenesis of cartilage degeneration in osteoarthritis (OA). However, little is known about the effect and underlying mechanism of berberine on OA chondrocytes. Here, we assessed the effects of berberine on cartilage degeneration in interleukin-1 (IL-1)-stimulated rat chondrocytes and in a rat model of OA. The results of an MTT assay and western blotting analysis showed that berberine attenuated the inhibitory effect of IL-1 on the cell viability and proliferating cell nuclear antigen expression in rat chondrocytes. Furthermore, berberine activated Akt, which triggered p70S6K/S6 pathway and up-regulated the levels of aggrecan and Col II expression in IL-1-stimulated rat chondrocytes. In addition, berberine increased the level of proteoglycans in cartilage matrix and the thickness of articular cartilage, with the elevated levels of Col II, p-Akt and p-S6 expression in a rat OA model, as demonstrated by histopathological and immunohistochemistry techniques. The data thus strongly suggest that berberine may ameliorate cartilage degeneration from OA by promoting cell survival and matrix production of chondrocytes, which was partly attributed to the activation of Akt in IL-1-stimulated articular chondrocytes and in a rat OA model. The resultant chondroprotective effects indicate that berberine merits consideration as a therapeutic agent in OA.