Abstract
Although safflower seed extract exhibits pharmacological activity against various diseases, the effects of its individual compounds on osteoarthritis (OA) have not been elucidated. Here, we evaluated the effects of these extracts and their single compounds on OA. N-(p-Coumaroyl) serotonin and N-feruloyl serotonin, main components of safflower seed extract, were isolated by high-performance liquid chromatography. Under in vitro OA mimic conditions, the expression of the matrix metalloproteinases (MMPs) MMP3/13 and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) ADAMTS5 were reduced in mouse chondrocytes treated with safflower seed extract. Furthermore, the oral administration of safflower seed extract attenuated cartilage destruction in a mouse OA model induced by destabilization of the medial meniscus. N-(p-Coumaroyl) serotonin and N-feruloyl serotonin, but not serotonin, reduced MMP3, MMP13, and ADAMTS5 expression in IL-1β-treated chondrocytes. Additionally, they significantly blocked the nuclear factor-κB (NF-κB) pathway by inhibiting IκB degradation and p65 phosphorylation. Our results suggest that safflower seed extract and its single compounds can attenuate cartilage destruction by suppressing MMP and ADMATS5 expression. The anti-arthritic effects are mediated by NF-κB signaling and involve the inhibition of IκB degradation and p65 phosphorylation. These results indicate that safflower seed extract may serve as a novel therapeutic agent against OA.
Highlights
We showed that N-feruloyl serotonin and N-(p-coumaroyl) serotonin prevented the development of OA
The results indicate that safflower seed extract has no toxicity against chondrocytes at the indicated concentrations; all subsequent experiments were performed at concentrations of 100, 200, and 400 μg/mL for 24 h
We previously showed that cartilage destruction is regulated by the expression of catabolic factors such as MMP3 and MMP13 [28,29]
Summary
Osteoarthritis (OA) is a common joint disease that can affect one or multiple joints [1]. The pathological features of OA include cartilage degradation, joint stiffness, pain, and swelling. The pathological mechanism of cartilage destruction in OA involves the upregulation of catabolic factors, such as matrix metalloproteinases (MMPs), the primary enzymes that promote cartilage degradation [2]. These catabolic factors are induced by proinflammatory cytokines such as IL-1β, which plays a pivotal role in cartilage destruction
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