Dataset Information

Curcumin Protects Osteoblasts From Oxidative Stress-Induced Dysfunction via GSK3?-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 (GSK3?) and activating nuclear factor erythroid 2 related factor 2 (Nrf2) could significantly antagonize the destructive effects of OS, which indicated the critical role of GSK3?-Nrf2 signaling. Furthermore, Cur also abolished the suppressive effects of OS on GSK3?-Nrf2 signaling pathway. Our findings demonstrated that Cur could protect osteoblasts against OS-induced dysfunction via GSK3?-Nrf2 signaling and provide a promising way for osteoporosis treatment.

SUBMITTER: Li X

PROVIDER: S-EPMC7308455 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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

Li Xumin X Chen Yang Y Mao Yixin Y Dai Panpan P Sun Xiaoyu X Zhang Xiaorong X Cheng Haoran H Wang Yingting Y Banda Isaac I Wu Gang G Ma Jianfeng J Huang Shengbin S Forouzanfar Tim T

Frontiers in bioengineering and biotechnology 20200616

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 m ...[more]

PMID: 32612986

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Project description:Oxidative stress is one of the main causes of osteoblast apoptosis induced by post-menopausal osteoporosis. The authors previously found that metformin can reverse the loss of bone mass in post-menopausal osteoporosis. The present study aimed to further clarify the effects and mechanisms of action of metformin in post-menopausal osteoporosis under conditions of oxidative stress. Combined with an in-depth investigation using the transcriptome database, the association between oxidative stress and mitochondrial dysfunction in post-menopausal osteoporosis was confirmed. A pre-osteoblast model of oxidative stress was constructed, and the apoptotic rate following the addition of hydrogen peroxide and metformin was detected using CCK-8 assay and Annexin V-FITC/PI staining. Mitochondrial membrane potential was detected using the JC-1 dye, the intracellular calcium concentration was detected using Fluo-4 AM, the intracellular reactive oxygen species (ROS) level was observed using DCFH-DA, and the mitochondrial superoxide level was observed using MitoSOX Red. Bay K8644 was used to increase the level of intracellular calcium. siRNA was used to interfere with the expression of glycogen synthase kinase (GSK)-3β. Western blot analysis was used to detect the expression of mitochondrial dysfunction-related proteins. The results revealed that oxidative stress decreased mitochondrial membrane potential and increased intracellular ROS, mitochondrial superoxide and cytoplasmic calcium levels in pre-osteoblasts; however, metformin improved mitochondrial dysfunction and reversed oxidative stress-induced injury. Metformin inhibited mitochondrial permeability transition pore opening, suppressed the cytoplasmic calcium influx and reversed pre-osteoblast apoptosis by promoting GSK-3β phosphorylation. Moreover, it was found that EGFR was the cell membrane receptor of metformin in pre-osteoblasts, and the EGFR/GSK-3β/calcium axis played a key role in metformin reversing the oxidative stress response of pre-osteoblasts in post-menopausal osteoporosis. On the whole, these findings provide a pharmacological basis for the use of metformin for the treatment of post-menopausal osteoporosis.

Dataset Information

Curcumin Protects Osteoblasts From Oxidative Stress-Induced Dysfunction via GSK3?-Nrf2 Signaling Pathway.

Publications

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

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