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Treatment with hydrogen molecules prevents RANKL-induced osteoclast differentiation associated with inhibition of ROS formation and inactivation of MAPK, AKT and NF-kappa B pathways in murine RAW264.7 cells.
J Bone Miner Metab. 2014 Sep; 32(5):494-504.JB

Abstract

The bone protective effects of the hydrogen molecule (H2) have been demonstrated in several osteoporosis models while the underlying molecular mechanism has remained unclear. Osteoclast differentiation is an important factor related to the pathogenesis of bone-loss related diseases. In this work, we evaluated the effects of incubation with H2 on receptor activator of NFκB ligand (RANKL)-induced osteoclast differentiation. We found that treatment with H2 prevented RANKL-induced osteoclast differentiation in RAW264.7 cells and BMMs. Treatment with H2 inhibits the ability to form resorption pits of BMMs stimulated by RANKL. Treatment with H2 reduced mRNA levels of osteoclast-specific markers including tartrate resistant acid phosphatase, calcitonin receptor, cathepsin K, metalloproteinase-9, carbonic anhydrase typeII, and vacuolar-type H(+)-ATPase. Treatment with H2 decreased intracellular reactive oxygen species (ROS) formation, suppressed NADPH oxidase activity, down-regulated Rac1 activity and Nox1 expression, reduced mitochondrial ROS formation, and enhanced nuclear factor E2-related factor 2 nuclear translocation and heme oxygenase-1 activity. In addition, treatment with H2 suppressed RANKL-induced expression of nuclear factor of activated T cells c1 and c-Fos. Furthermore, treatment with H2 suppressed NF-κB activation and reduced phosphorylation of p38, extracellular signal-regulated kinase, c-Jun-N-terminal kinase, and protein kinases B (AKT) stimulated with RANKL. In conclusion, hydrogen molecules prevented RANKL-induced osteoclast differentiation associated with inhibition of reactive oxygen species formation and inactivation of NF-κB, mitogen-activated protein kinase and AKT pathways.

Authors+Show Affiliations

Department of Osteology, The 89th Hospital of The Chinese PLA, 256 Beigong West Street, Weifang, 261021, China, lidongzhu2013@hotmail.com.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

24196871

Citation

Li, Dong-Zhu, et al. "Treatment With Hydrogen Molecules Prevents RANKL-induced Osteoclast Differentiation Associated With Inhibition of ROS Formation and Inactivation of MAPK, AKT and NF-kappa B Pathways in Murine RAW264.7 Cells." Journal of Bone and Mineral Metabolism, vol. 32, no. 5, 2014, pp. 494-504.
Li DZ, Zhang QX, Dong XX, et al. Treatment with hydrogen molecules prevents RANKL-induced osteoclast differentiation associated with inhibition of ROS formation and inactivation of MAPK, AKT and NF-kappa B pathways in murine RAW264.7 cells. J Bone Miner Metab. 2014;32(5):494-504.
Li, D. Z., Zhang, Q. X., Dong, X. X., Li, H. D., & Ma, X. (2014). Treatment with hydrogen molecules prevents RANKL-induced osteoclast differentiation associated with inhibition of ROS formation and inactivation of MAPK, AKT and NF-kappa B pathways in murine RAW264.7 cells. Journal of Bone and Mineral Metabolism, 32(5), 494-504. https://doi.org/10.1007/s00774-013-0530-1
Li DZ, et al. Treatment With Hydrogen Molecules Prevents RANKL-induced Osteoclast Differentiation Associated With Inhibition of ROS Formation and Inactivation of MAPK, AKT and NF-kappa B Pathways in Murine RAW264.7 Cells. J Bone Miner Metab. 2014;32(5):494-504. PubMed PMID: 24196871.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Treatment with hydrogen molecules prevents RANKL-induced osteoclast differentiation associated with inhibition of ROS formation and inactivation of MAPK, AKT and NF-kappa B pathways in murine RAW264.7 cells. AU - Li,Dong-Zhu, AU - Zhang,Qing-Xiang, AU - Dong,Xiao-Xian, AU - Li,Huai-Dong, AU - Ma,Xin, Y1 - 2013/11/07/ PY - 2013/05/01/received PY - 2013/10/09/accepted PY - 2013/11/8/entrez PY - 2013/11/8/pubmed PY - 2015/5/16/medline SP - 494 EP - 504 JF - Journal of bone and mineral metabolism JO - J. Bone Miner. Metab. VL - 32 IS - 5 N2 - The bone protective effects of the hydrogen molecule (H2) have been demonstrated in several osteoporosis models while the underlying molecular mechanism has remained unclear. Osteoclast differentiation is an important factor related to the pathogenesis of bone-loss related diseases. In this work, we evaluated the effects of incubation with H2 on receptor activator of NFκB ligand (RANKL)-induced osteoclast differentiation. We found that treatment with H2 prevented RANKL-induced osteoclast differentiation in RAW264.7 cells and BMMs. Treatment with H2 inhibits the ability to form resorption pits of BMMs stimulated by RANKL. Treatment with H2 reduced mRNA levels of osteoclast-specific markers including tartrate resistant acid phosphatase, calcitonin receptor, cathepsin K, metalloproteinase-9, carbonic anhydrase typeII, and vacuolar-type H(+)-ATPase. Treatment with H2 decreased intracellular reactive oxygen species (ROS) formation, suppressed NADPH oxidase activity, down-regulated Rac1 activity and Nox1 expression, reduced mitochondrial ROS formation, and enhanced nuclear factor E2-related factor 2 nuclear translocation and heme oxygenase-1 activity. In addition, treatment with H2 suppressed RANKL-induced expression of nuclear factor of activated T cells c1 and c-Fos. Furthermore, treatment with H2 suppressed NF-κB activation and reduced phosphorylation of p38, extracellular signal-regulated kinase, c-Jun-N-terminal kinase, and protein kinases B (AKT) stimulated with RANKL. In conclusion, hydrogen molecules prevented RANKL-induced osteoclast differentiation associated with inhibition of reactive oxygen species formation and inactivation of NF-κB, mitogen-activated protein kinase and AKT pathways. SN - 1435-5604 UR - https://www.unboundmedicine.com/medline/citation/24196871/Treatment_with_hydrogen_molecules_prevents_RANKL_induced_osteoclast_differentiation_associated_with_inhibition_of_ROS_formation_and_inactivation_of_MAPK_AKT_and_NF_kappa_B_pathways_in_murine_RAW264_7_cells_ L2 - https://dx.doi.org/10.1007/s00774-013-0530-1 DB - PRIME DP - Unbound Medicine ER -