Abstract
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.
Highlights
One of the main symptoms in osteoarthritis (OA) is the progressive degeneration of articular cartilage including chondrocyte loss and degradation of the extracellular matrix (ECM) [1]
The purpose of this study is to investigate the effect of berberine on IL-1b-stimulated rat chondrocytes, as well as articular cartilage in a rat OA model, and to elucidate the underlying mechanism associated with Akt signalling
We found that berberine promoted chondrocyte survival and matrix production in IL-1b-stimulated articular chondrocytes, one type of model OA chondrocytes, and in a rat model of OA
Summary
One of the main symptoms in osteoarthritis (OA) is the progressive degeneration of articular cartilage including chondrocyte loss and degradation of the extracellular matrix (ECM) [1]. Chondrocyte apoptosis that is higher in human OA cartilage could be involved in the initiation and severity of articular cartilage degeneration [2, 3]. Proinflammatory cytokines secreted by chondrocytes, such as interleukin-1b (IL-1b) and tumour necrosis factor-a, contribute to the progression of OA [7,8,9]. IL-1b can trigger chondrocyte apoptosis and is commonly used as a modulating and chondrocyte apoptosisinducing agent [10,11,12]. The chondrocytes treated with IL-1b mimicked OA chondrocytes [11, 12]
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