Department of Orthopedics, Nanjing Medical University Affiliated Wuxi Second Hospital, Wuxi, 214002, Jiangsu, China.
Inflamm Res. 2017 Dec;66(12):1075-1084. doi: 10.1007/s00011-017-1087-6. Epub 2017 Aug 29.
Malvidin is one of the most widespread anthocyanidins which exhibits significant antioxidant and anti-inflammatory activity. The aim of this paper is to investigate the effects of Malvidin on osteoarthritis (OA).
We created an animal model of OA using Wistar rats administered by monosodium iodoacetate (MIA). Effects of Malvidin on hyperalgesia were evaluated by paw pressure tests and compression threshold test. Articular chondrocytes were isolated from the OA rats to detect the apoptotic chondrocytes using senescence-associated β-galactosidase (SA-β-gal) staining kit. The expression levels of pro-inflammatory cytokines and matrix metalloproteinase (MMPs) were assessed by western blot and qPCR. Luciferase assay was used to determine the impact of Malvidin on nuclear factor-kappa B (NF-κB) pathway.
Malvidin treatment exhibited significant pain-relieving effects in OA rats and decreased the expression level of apoptotic marker SA-β-gal in chondrocytes. We found that the upregulated expressions of interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), and MMPs induced by MIA in cartilage tissues were significantly reversed by Malvidin. Furthermore, Malvidin inhibited NF-κB pathway via an NF-κB inhibitor (IκBα)-independent manner through suppressing p65 nuclear transportation in vitro.
Our findings suggest that Malvidin significantly attenuates the OA-induced pain and inflammation by inhibiting NF-κB signaling pathway and suppressing pro-inflammatory cytokine expression and chondrocyte apoptosis.
矢车菊素是分布最广泛的花色苷之一，具有显著的抗氧化和抗炎活性。本文旨在研究矢车菊素对骨关节炎（OA）的影响。
我们使用单碘乙酸盐（MIA）处理 Wistar 大鼠建立 OA 动物模型。通过爪压力测试和压缩阈值测试评估矢车菊素对痛觉过敏的影响。从 OA 大鼠中分离关节软骨细胞，使用衰老相关β-半乳糖苷酶（SA-β-半乳糖苷）染色试剂盒检测凋亡软骨细胞。通过 Western blot 和 qPCR 评估促炎细胞因子和基质金属蛋白酶（MMPs）的表达水平。使用荧光素酶测定法确定矢车菊素对核因子-κB（NF-κB）途径的影响。
矢车菊素治疗可显著减轻 OA 大鼠的疼痛，并降低软骨细胞中凋亡标志物 SA-β-半乳糖苷的表达水平。我们发现，MIA 诱导的软骨组织中白细胞介素（IL）-1β、IL-6、肿瘤坏死因子-α（TNF-α）和 MMPs 的上调表达，均被矢车菊素显著逆转。此外，矢车菊素通过抑制 p65 核转运，以 IκBα 非依赖性方式抑制 NF-κB 通路，从而在体外抑制 NF-κB 信号通路。
我们的研究结果表明，矢车菊素通过抑制 NF-κB 信号通路和抑制促炎细胞因子表达和软骨细胞凋亡，显著减轻 OA 引起的疼痛和炎症。
