Zhongshan Hospital, University of Xiamen, Xiamen, Fujian, China.
J Cell Mol Med. 2014 Feb;18(2):283-92. doi: 10.1111/jcmm.12186. Epub 2013 Nov 28.
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-1β (IL-1β)-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-1β 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-1β-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-1β-stimulated articular chondrocytes and in a rat OA model. The resultant chondroprotective effects indicate that berberine merits consideration as a therapeutic agent in OA.
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功能。软骨细胞凋亡是骨关节炎（OA）软骨退变的发病机制之一。然而，小檗碱对 OA 软骨细胞的作用及其潜在机制知之甚少。在这里，我们评估了小檗碱对白细胞介素-1β（IL-1β）刺激的大鼠软骨细胞和大鼠 OA 模型中软骨退变的影响。MTT 检测和 Western blot 分析结果表明，小檗碱可减弱 IL-1β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，并上调 IL-1β刺激的大鼠软骨细胞中聚集蛋白聚糖和 Col II 的表达水平。此外，小檗碱增加了软骨基质中糖胺聚糖的水平和关节软骨的厚度，在大鼠 OA 模型中，Col II、p-Akt 和 p-S6 的表达水平升高，这通过组织病理学和免疫组织化学技术得到证实。这些数据强烈表明，小檗碱可能通过促进软骨细胞的存活和基质产生来改善 OA 引起的软骨退变，这部分归因于 IL-1β刺激的关节软骨细胞和大鼠 OA 模型中 Akt 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 的治疗药物。
