Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Department of Orthopedics, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei 441021, China.
Food Funct. 2020 Sep 23;11(9):7935-7945. doi: 10.1039/d0fo01496f.
Osteoarthritis (OA) is a common joint disease characterized by cartilage degeneration and inflammation. Although moracin is known to play a role in anti-inflammation and anti-oxidation in several inflammatory diseases, its anti-inflammatory effect on OA remains largely unknown. Therefore, in order to explore the role of moracin in OA, we investigated the anti-inflammatory effect of moracin on interleukin (IL)-β-induced rat chondrocytes in vitro and surgically induced OA rat models in vivo. Rat chondrocytes were pretreated using moracin (0, 5, 10, 15 μmol L-1) and then stimulated with IL-β (10 ng ml-1). Results showed that moracin reduced the expression of IL-1β-induced nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), IL-6, inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX)-2 in both rat chondrocytes and cell culture supernatants. Besides, IL-1β-induced degradation of aggrecan and collage II, and the high expression of matrix metalloproteinase-13 (MMP-13) and a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS)-5 were also reversed by moracin. Moreover, moracin inhibited the translocation of p65 from the cytoplasm to nucleus induced by IL-1β and activated the Nrf2/HO-1 signaling pathway in chondrocytes. In OA rat models, moracin prevented cartilage of rats from destruction. All these findings above indicated that moracin could be a potentially effective drug for treating OA.
骨关节炎（OA）是一种常见的关节疾病，其特征为软骨退化和炎症。虽然众所周知，moracin 在几种炎症性疾病中具有抗炎和抗氧化作用，但它对 OA 的抗炎作用在很大程度上尚不清楚。因此，为了探讨 moracin 在 OA 中的作用，我们在体外研究了 moracin 对白细胞介素（IL）-β诱导的大鼠软骨细胞的抗炎作用，以及体内手术诱导的 OA 大鼠模型。用 moracin（0、5、10、15 μmol L-1）预处理大鼠软骨细胞，然后用 IL-β（10 ng ml-1）刺激。结果表明，moracin 降低了 IL-1β诱导的一氧化氮（NO）、前列腺素 E2（PGE2）、肿瘤坏死因子-α（TNF-α）、IL-6、诱导型一氧化氮合酶（iNOS）和环氧化酶（COX）-2在大鼠软骨细胞和细胞培养上清液中的表达。此外，moracin 还逆转了 IL-1β诱导的聚集蛋白聚糖和胶原 II 的降解，以及基质金属蛋白酶-13（MMP-13）和含有血栓反应蛋白 1 型金属蛋白酶结构域 5（ADAMTS）-5 的高表达。此外，moracin 抑制了 IL-1β诱导的 p65 从细胞质向细胞核的易位，并激活了软骨细胞中的 Nrf2/HO-1 信号通路。在 OA 大鼠模型中，moracin 防止了大鼠软骨的破坏。所有这些发现表明，moracin 可能是治疗 OA 的一种潜在有效药物。
