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

Aims: Tert-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. Methods: OA animal model...

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Autores principales:	Hua Zhang, Jie Li, Xiaobing Xiang, Bengen Zhou, Changqing Zhao, Qiushi Wei, Youqiang Sun, Jianfa Chen, Boyong Lai, Zequan Luo, Aihua Li
Formato:	article
Lenguaje:	EN
Publicado:	The British Editorial Society of Bone & Joint Surgery 2021
Materias:	tbhq osteoarthritis apoptosis osteoarthritis (oa) chondrocytes macrophages interleukin 6 inflammation interleukin 1 beta western blot blood destabilization of the medial meniscus (dmm) Diseases of the musculoskeletal system RC925-935
Acceso en línea:	https://doaj.org/article/ec12cef9b5944ccfb9b167cbd83357f4
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spelling	oai:doaj.org-article:ec12cef9b5944ccfb9b167cbd83357f42021-12-01T18:46:59ZTert-butylhydroquinone attenuates osteoarthritis by protecting chondrocytes and inhibiting macrophage polarization2046-375810.1302/2046-3758.1011.BJR-2020-0242.R4https://doaj.org/article/ec12cef9b5944ccfb9b167cbd83357f42021-11-01T00:00:00Zhttps://online.boneandjoint.org.uk/doi/epdf/10.1302/2046-3758.1011.BJR-2020-0242.R4https://doaj.org/toc/2046-3758Aims: Tert-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. Methods: OA 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. Results: Tert-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. Conclusion: Taken together, tBHQ might be a potential therapeutic strategy for protecting against OA development. Cite this article: Bone Joint Res 2021;10(11):704–713.Hua ZhangJie LiXiaobing XiangBengen ZhouChangqing ZhaoQiushi WeiYouqiang SunJianfa ChenBoyong LaiZequan LuoAihua LiThe British Editorial Society of Bone & Joint Surgeryarticletbhqosteoarthritisapoptosisosteoarthritis (oa)chondrocytesmacrophagesinterleukin 6apoptosisinflammationinterleukin 1 betawestern blotblooddestabilization of the medial meniscus (dmm)Diseases of the musculoskeletal systemRC925-935ENBone & Joint Research, Vol 10, Iss 11, Pp 704-713 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	tbhq osteoarthritis apoptosis osteoarthritis (oa) chondrocytes macrophages interleukin 6 apoptosis inflammation interleukin 1 beta western blot blood destabilization of the medial meniscus (dmm) Diseases of the musculoskeletal system RC925-935
spellingShingle	tbhq osteoarthritis apoptosis osteoarthritis (oa) chondrocytes macrophages interleukin 6 apoptosis inflammation interleukin 1 beta western blot blood destabilization of the medial meniscus (dmm) Diseases of the musculoskeletal system RC925-935 Hua Zhang Jie Li Xiaobing Xiang Bengen Zhou Changqing Zhao Qiushi Wei Youqiang Sun Jianfa Chen Boyong Lai Zequan Luo Aihua Li Tert-butylhydroquinone attenuates osteoarthritis by protecting chondrocytes and inhibiting macrophage polarization
description	Aims: Tert-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. Methods: OA 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. Results: Tert-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. Conclusion: Taken together, tBHQ might be a potential therapeutic strategy for protecting against OA development. Cite this article: Bone Joint Res 2021;10(11):704–713.
format	article
author	Hua Zhang Jie Li Xiaobing Xiang Bengen Zhou Changqing Zhao Qiushi Wei Youqiang Sun Jianfa Chen Boyong Lai Zequan Luo Aihua Li
author_facet	Hua Zhang Jie Li Xiaobing Xiang Bengen Zhou Changqing Zhao Qiushi Wei Youqiang Sun Jianfa Chen Boyong Lai Zequan Luo Aihua Li
author_sort	Hua Zhang
title	Tert-butylhydroquinone attenuates osteoarthritis by protecting chondrocytes and inhibiting macrophage polarization
title_short	Tert-butylhydroquinone attenuates osteoarthritis by protecting chondrocytes and inhibiting macrophage polarization
title_full	Tert-butylhydroquinone attenuates osteoarthritis by protecting chondrocytes and inhibiting macrophage polarization
title_fullStr	Tert-butylhydroquinone attenuates osteoarthritis by protecting chondrocytes and inhibiting macrophage polarization
title_full_unstemmed	Tert-butylhydroquinone attenuates osteoarthritis by protecting chondrocytes and inhibiting macrophage polarization
title_sort	tert-butylhydroquinone attenuates osteoarthritis by protecting chondrocytes and inhibiting macrophage polarization
publisher	The British Editorial Society of Bone & Joint Surgery
publishDate	2021
url	https://doaj.org/article/ec12cef9b5944ccfb9b167cbd83357f4
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Tert-butylhydroquinone attenuates osteoarthritis by protecting chondrocytes and inhibiting macrophage polarization

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