Tert-butylhydroquinone attenuates osteoarthritis by protecting chondrocytes and inhibiting macrophage polarization

Bone & Joint Research

article

Hua Zhang¹  Jie Li¹  Xiaobing Xiang¹  Bengen Zhou¹  Changqing Zhao¹  Qiushi Wei¹  Youqiang Sun¹  Jianfa Chen¹  Boyong Lai¹  Zequan Luo¹  Aihua Li¹ 

[1] Department of Orthopedics, The First Affiliated Hospital of Guangzhou University of Traditional Chinese Medicine

关键词: tBHQ;    Osteoarthritis;    Apoptosis;    Osteoarthritis (OA);    Chondrocytes;    macrophages;    interleukin 6;    apoptosis;    inflammation;    interleukin 1 beta;    western blot;    blood;    destabilization of the medial meniscus (DMM);   

DOI  :  10.1302/2046-3758.1011.BJR-2020-0242.R4

学科分类：骨科学

来源: British Editorial Society Of Bone And Joint Surgery

【 摘 要 】

AimsTert-butylhydroquinone (tBHQ) has been identified as an inhibitor of oxidative stress-induced injury and apoptosis in human neural stem cells. However, the role of tBHQ in osteoarthritis (OA) is unclear. This study was carried out to investigate the role of tBHQ in OA.MethodsOA animal model was induced by destabilization of the medial meniscus (DMM). Different concentrations of tBHQ (25 and 50 mg/kg) were intraperitoneally injected in ten-week-old female mice. Chondrocytes were isolated from articular cartilage of mice and treated with 5 ng/ml lipopolysaccharide (LPS) or 10 ng/ml interleukin 1 beta (IL-1β) for 24 hours, and then treated with different concentrations of tBHQ (10, 20, and 40 μM) for 12 hours. The expression levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in blood were measured. The expression levels of interleukin 6 (IL-6), IL-1β, and tumour necrosis factor alpha (TNF-α) leptin in plasma were measured using enzyme-linked immunoabsorbent assay (ELISA) kits. The expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathway proteins, and macrophage repolarization-related markers, were detected by western blot.ResultsTert-butylhydroquinone significantly attenuated cartilage destruction in DMM-induced mice in vivo. It demonstrated clear evidence of inhibiting IL-1β-induced chondrocyte apoptosis, inflammation, and differentiation defect in vitro. Meanwhile, tBHQ inhibited LPS-induced activation of NF-κB and MAPK signalling pathways, and also inhibited LPS-induced reactive oxygen species production and macrophages repolarization in vitro.ConclusionTaken together, tBHQ might be a potential therapeutic strategy for protecting against OA development.

【 授权许可】

CC BY-NC