Curcumin Protects Osteoblasts From Oxidative Stress-Induced Dysfunction via GSK3β-Nrf2 Signaling Pathway

X. Li; Y. Chen; Y. Mao; P. Dai; X. Sun; X. Zhang; H. Cheng; Y. Wang; I. Banda; G. Wu; J. Ma; S. Huang; T. Forouzanfar

doi:10.3389/fbioe.2020.00625

Curcumin Protects Osteoblasts From Oxidative Stress-Induced Dysfunction via GSK3β-Nrf2 Signaling Pathway

X. Li
, Y. Chen
, Y. Mao
, P. Dai
, X. Sun
, X. Zhang
, H. Cheng
, Y. Wang
, I. Banda
, G. Wu
, J. Ma
, S. Huang
, T. Forouzanfar

Research output: Contribution to Journal › Article › Academic › peer-review

Abstract

Osteoblasts dysfunction, induced by oxidative stress (OS), is one of major pathological mechanisms for osteoporosis. Curcumin (Cur), a bioactive antioxidant compound, isolated from Curcumin longa L, was regarded as a strong reactive oxygen species (ROS) scavenger. However, it remains unveiled whether Cur can prevent osteoblasts from OS-induced dysfunction. To approach this question, we adopted a well-established OS model to investigate the preventive effect of Cur on osteoblasts dysfunction by measuring intracellular ROS production, cell viability, apoptosis rate and osteoblastogenesis markers. We showed that the pretreatment of Cur could significantly antagonize OS so as to suppress endogenous ROS production, maintain osteoblasts viability and promote osteoblastogenesis. Inhibiting Glycogen synthase kinase (GSK3β) and activating nuclear factor erythroid 2 related factor 2 (Nrf2) could significantly antagonize the destructive effects of OS, which indicated the critical role of GSK3β-Nrf2 signaling. Furthermore, Cur also abolished the suppressive effects of OS on GSK3β-Nrf2 signaling pathway. Our findings demonstrated that Cur could protect osteoblasts against OS-induced dysfunction via GSK3β-Nrf2 signaling and provide a promising way for osteoporosis treatment.

Original language	English
Article number	625
Pages (from-to)	1-13
Number of pages	13
Journal	Frontiers in Bioengineering and Biotechnology
Volume	8
Issue number	June
Early online date	16 Jun 2020
DOIs	https://doi.org/10.3389/fbioe.2020.00625
Publication status	Published - Jun 2020

Funding

This project was funded by Science and Technology Project of Zhejiang Province (No. 2017C33081), National Natural Science Foundation of China (No. 81870777), Natural Science Foundation of Zhejiang Province (No. LY17H140010), Traditional Chinese Medicine Science and Technology Program of Zhejiang Province (No. 2019ZB077), Wenzhou Technology Bureau Project (No. 2018Y0724), Orthopedics Key Laboratory Open Fund of Zhejiang Province (No. ZJGK1807Y), China Scholarship Council (No. 201808330402), and Zhejiang Provincial College Students’ Science and Technology Innovation Project and Fresh Talent Program (Nos. 2019R413059 and 2019R413084). The funders had no role in study design, data collection, and analysis, the decision to publish, or the preparation of the manuscript.

Funders	Funder number
Orthopedics Key Laboratory Open Fund of Zhejiang Province	ZJGK1807Y
Traditional Chinese Medicine Science and Technology Program of Zhejiang Province	2019ZB077
Wenzhou Technology Bureau Project	2018Y0724
Zhejiang Provincial College Students’ Science and Technology Innovation Project and Fresh Talent Program	2019R413084, 2019R413059
National Natural Science Foundation of China	81870777
China Scholarship Council	201808330402
Natural Science Foundation of Zhejiang Province	LY17H140010
Science and Technology Program of Zhejiang Province	2017C33081

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10.3389/fbioe.2020.00625

https://hdl.handle.net/11245.1/8c9b1313-685b-4d5f-aaeb-442e6fbaf579

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@article{c8926d5642034f7a879478ff959af0df,

title = "Curcumin Protects Osteoblasts From Oxidative Stress-Induced Dysfunction via GSK3β-Nrf2 Signaling Pathway",

abstract = "Osteoblasts dysfunction, induced by oxidative stress (OS), is one of major pathological mechanisms for osteoporosis. Curcumin (Cur), a bioactive antioxidant compound, isolated from Curcumin longa L, was regarded as a strong reactive oxygen species (ROS) scavenger. However, it remains unveiled whether Cur can prevent osteoblasts from OS-induced dysfunction. To approach this question, we adopted a well-established OS model to investigate the preventive effect of Cur on osteoblasts dysfunction by measuring intracellular ROS production, cell viability, apoptosis rate and osteoblastogenesis markers. We showed that the pretreatment of Cur could significantly antagonize OS so as to suppress endogenous ROS production, maintain osteoblasts viability and promote osteoblastogenesis. Inhibiting Glycogen synthase kinase (GSK3β) and activating nuclear factor erythroid 2 related factor 2 (Nrf2) could significantly antagonize the destructive effects of OS, which indicated the critical role of GSK3β-Nrf2 signaling. Furthermore, Cur also abolished the suppressive effects of OS on GSK3β-Nrf2 signaling pathway. Our findings demonstrated that Cur could protect osteoblasts against OS-induced dysfunction via GSK3β-Nrf2 signaling and provide a promising way for osteoporosis treatment.",

author = "X. Li and Y. Chen and Y. Mao and P. Dai and X. Sun and X. Zhang and H. Cheng and Y. Wang and I. Banda and G. Wu and J. Ma and S. Huang and T. Forouzanfar",

year = "2020",

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AU - Li, X.

AU - Chen, Y.

AU - Mao, Y.

AU - Dai, P.

AU - Sun, X.

AU - Zhang, X.

AU - Cheng, H.

AU - Wang, Y.

AU - Banda, I.

AU - Wu, G.

AU - Ma, J.

AU - Huang, S.

AU - Forouzanfar, T.

PY - 2020/6

Y1 - 2020/6

N2 - Osteoblasts dysfunction, induced by oxidative stress (OS), is one of major pathological mechanisms for osteoporosis. Curcumin (Cur), a bioactive antioxidant compound, isolated from Curcumin longa L, was regarded as a strong reactive oxygen species (ROS) scavenger. However, it remains unveiled whether Cur can prevent osteoblasts from OS-induced dysfunction. To approach this question, we adopted a well-established OS model to investigate the preventive effect of Cur on osteoblasts dysfunction by measuring intracellular ROS production, cell viability, apoptosis rate and osteoblastogenesis markers. We showed that the pretreatment of Cur could significantly antagonize OS so as to suppress endogenous ROS production, maintain osteoblasts viability and promote osteoblastogenesis. Inhibiting Glycogen synthase kinase (GSK3β) and activating nuclear factor erythroid 2 related factor 2 (Nrf2) could significantly antagonize the destructive effects of OS, which indicated the critical role of GSK3β-Nrf2 signaling. Furthermore, Cur also abolished the suppressive effects of OS on GSK3β-Nrf2 signaling pathway. Our findings demonstrated that Cur could protect osteoblasts against OS-induced dysfunction via GSK3β-Nrf2 signaling and provide a promising way for osteoporosis treatment.

AB - Osteoblasts dysfunction, induced by oxidative stress (OS), is one of major pathological mechanisms for osteoporosis. Curcumin (Cur), a bioactive antioxidant compound, isolated from Curcumin longa L, was regarded as a strong reactive oxygen species (ROS) scavenger. However, it remains unveiled whether Cur can prevent osteoblasts from OS-induced dysfunction. To approach this question, we adopted a well-established OS model to investigate the preventive effect of Cur on osteoblasts dysfunction by measuring intracellular ROS production, cell viability, apoptosis rate and osteoblastogenesis markers. We showed that the pretreatment of Cur could significantly antagonize OS so as to suppress endogenous ROS production, maintain osteoblasts viability and promote osteoblastogenesis. Inhibiting Glycogen synthase kinase (GSK3β) and activating nuclear factor erythroid 2 related factor 2 (Nrf2) could significantly antagonize the destructive effects of OS, which indicated the critical role of GSK3β-Nrf2 signaling. Furthermore, Cur also abolished the suppressive effects of OS on GSK3β-Nrf2 signaling pathway. Our findings demonstrated that Cur could protect osteoblasts against OS-induced dysfunction via GSK3β-Nrf2 signaling and provide a promising way for osteoporosis treatment.

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Curcumin Protects Osteoblasts From Oxidative Stress-Induced Dysfunction via GSK3β-Nrf2 Signaling Pathway

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