Department of Orthopaedic Surgery, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.
Department of Chemoradiation Oncology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
J Cell Mol Med. 2019 Mar;23(3):1940-1950. doi: 10.1111/jcmm.14096. Epub 2019 Jan 3.
The anti-inflammatory effect of sinapic acid (SA) has been reported in several studies. However, whether SA has the same effect on osteoarthritis (OA) has yet to be clearly elucidated. We designed a series of in vitro and in vivo procedures to verify the above conjecture. Compared with controls, SA-pretreated human chondrocytes showed lower levels of interleukin (IL)-1β-induced IL-6, prostaglandin E2 (PGE2), nitric oxide (NO) and tumour necrosis factor-α (TNF-α) in vitro. Meanwhile, SA could also reverse the degradation of type II collage and aggrecan, as well as the overproduction of matrix metalloproteinase-9 (MMP-9) and matrix metalloproteinase-13 (MMP-13), inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2 and a disintegrin and metalloproteinase thrombospondin motifs (ADAMTS)-5. Furthermore, activation of nuclear factor κB (NF-κB), which was induced by IL-1β, was also inhibited by SA through the pathway of nuclear factor-erythroid 2-related factor-2 (Nrf2)/heme oxygenase 1. In vivo, SA could delay the progress of mice OA models. We propose that SA may be applied as a potential therapeutic drug in OA treatment.
咖啡酸(SA)的抗炎作用已在多项研究中得到报道。然而,SA 对骨关节炎(OA)是否具有相同的作用尚未得到明确阐明。我们设计了一系列体外和体内程序来验证上述推测。与对照组相比,SA 预处理的人软骨细胞在体外表现出较低水平的白细胞介素(IL)-1β诱导的 IL-6、前列腺素 E2(PGE2)、一氧化氮(NO)和肿瘤坏死因子-α(TNF-α)。同时,SA 还可以逆转 II 型胶原和聚集蛋白聚糖的降解,以及基质金属蛋白酶-9(MMP-9)和基质金属蛋白酶-13(MMP-13)、诱导型一氧化氮合酶(iNOS)、环氧化酶(COX)-2 和金属蛋白酶金属蛋白酶组织抑制剂-1(TIMP-1)的过度产生。此外,SA 通过核因子-红细胞 2 相关因子-2(Nrf2)/血红素加氧酶 1 途径抑制 IL-1β诱导的核因子 κB(NF-κB)的激活。在体内,SA 可以延缓小鼠 OA 模型的进展。我们提出,SA 可能被用作 OA 治疗的潜在治疗药物。