Dextromethorphan Inhibits Osteoblast Differentiation and Bone Regeneration of Rats With Subcritical-Sized Calvarial Defects.
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Environmental toxicology
2025
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| author | Lai, Yu-Cheng Yao, Zhi-Kang Chang, Tien-Chieh Feng, Chien-Wei Kuo, Tsu-Jen Luo, Yi-Wei Jean, Yen-Hsuan Lin, Hugo Y-H Wen, Zhi-Hong |
| author_facet | Lai, Yu-Cheng Yao, Zhi-Kang Chang, Tien-Chieh Feng, Chien-Wei Kuo, Tsu-Jen Luo, Yi-Wei Jean, Yen-Hsuan Lin, Hugo Y-H Wen, Zhi-Hong Lai, Yu-Cheng Yao, Zhi-Kang Chang, Tien-Chieh Feng, Chien-Wei Kuo, Tsu-Jen Luo, Yi-Wei Jean, Yen-Hsuan Lin, Hugo Y-H Wen, Zhi-Hong |
| collection | PubMed - marine biology |
| contents | Dextromethorphan Inhibits Osteoblast Differentiation and Bone Regeneration of Rats With Subcritical-Sized Calvarial Defects. Lai, Yu-Cheng Yao, Zhi-Kang Chang, Tien-Chieh Feng, Chien-Wei Kuo, Tsu-Jen Luo, Yi-Wei Jean, Yen-Hsuan Lin, Hugo Y-H Wen, Zhi-Hong Animals Bone Regeneration Osteoblasts Dextromethorphan Cell Differentiation Skull Mice Osteogenesis Rats Zebrafish Cell Line Male Rats, Sprague-Dawley Osteocalcin Core Binding Factor Alpha 1 Subunit The glutamatergic signaling pathway, which is mediated by N-methyl-D-aspartate (NMDA) receptors, is crucial for osteoblast differentiation and bone function. Dextromethorphan (DXM), a widely used antitussive, is a noncompetitive antagonist of the NMDA receptor. However, the effects of DXM on osteoblast and bone regeneration remain unclear. The present study investigated the effects of DXM on osteogenesis in vitro and in vivo. A MC3T3-E1 preosteoblast cell line was treated with varying concentrations of DXM. Real-time-quantitative polymerase chain reaction (RT-qPCR) and Western-blot analysis were performed to evaluate the expression of osteogenesis-related runt-related transcription factor 2 (RUNX2), osterix (OSX), osteocalcin (OCN), collagen type 1α (Col-1α), and alkaline phosphatase (ALP) after DXM treatment. Zebrafish embryos were incubated with DXM, which had potential to affect the ossification of the vertebrae and skull, and analyzed using calcein staining. Furthermore, we used a rat calvarial defect model to assess the effects of DXM on bone regeneration by using microcomputed tomography. The results indicate that DXM inhibited extracellular mineralization, ALP activity, and the expression of osteogenic markers, namely RUNX2, OSX, OCN, Col-1α, and ALP, in MC3T3-E1 cells. DXM suppressed skeleton ossification in zebrafish and affected bone regeneration in rats with calvarial defects. However, the mineral density of the regenerated bones did not differ significantly between the DXM and control groups. The present study demonstrated that DXM negatively affects the osteogenic function of osteoblasts, leading to impaired skeletal development and bone regeneration. Thus, clinicians should consider the negative effects of DXM on bone regeneration. |
| format | Artículo científico |
| id | pubmed_39607004 |
| institution | PubMed |
| language | en |
| publishDate | 2025 |
| publisher | Environmental toxicology |
| record_format | pubmed |
| spellingShingle | Dextromethorphan Inhibits Osteoblast Differentiation and Bone Regeneration of Rats With Subcritical-Sized Calvarial Defects. Lai, Yu-Cheng Yao, Zhi-Kang Chang, Tien-Chieh Feng, Chien-Wei Kuo, Tsu-Jen Luo, Yi-Wei Jean, Yen-Hsuan Lin, Hugo Y-H Wen, Zhi-Hong Animals Bone Regeneration Osteoblasts Dextromethorphan Cell Differentiation Skull Mice Osteogenesis Rats Zebrafish Cell Line Male Rats, Sprague-Dawley Osteocalcin Core Binding Factor Alpha 1 Subunit Dextromethorphan Inhibits Osteoblast Differentiation and Bone Regeneration of Rats With Subcritical-Sized Calvarial Defects. Lai, Yu-Cheng Yao, Zhi-Kang Chang, Tien-Chieh Feng, Chien-Wei Kuo, Tsu-Jen Luo, Yi-Wei Jean, Yen-Hsuan Lin, Hugo Y-H Wen, Zhi-Hong Animals Bone Regeneration Osteoblasts Dextromethorphan Cell Differentiation Skull Mice Osteogenesis Rats Zebrafish Cell Line Male Rats, Sprague-Dawley Osteocalcin Core Binding Factor Alpha 1 Subunit The glutamatergic signaling pathway, which is mediated by N-methyl-D-aspartate (NMDA) receptors, is crucial for osteoblast differentiation and bone function. Dextromethorphan (DXM), a widely used antitussive, is a noncompetitive antagonist of the NMDA receptor. However, the effects of DXM on osteoblast and bone regeneration remain unclear. The present study investigated the effects of DXM on osteogenesis in vitro and in vivo. A MC3T3-E1 preosteoblast cell line was treated with varying concentrations of DXM. Real-time-quantitative polymerase chain reaction (RT-qPCR) and Western-blot analysis were performed to evaluate the expression of osteogenesis-related runt-related transcription factor 2 (RUNX2), osterix (OSX), osteocalcin (OCN), collagen type 1α (Col-1α), and alkaline phosphatase (ALP) after DXM treatment. Zebrafish embryos were incubated with DXM, which had potential to affect the ossification of the vertebrae and skull, and analyzed using calcein staining. Furthermore, we used a rat calvarial defect model to assess the effects of DXM on bone regeneration by using microcomputed tomography. The results indicate that DXM inhibited extracellular mineralization, ALP activity, and the expression of osteogenic markers, namely RUNX2, OSX, OCN, Col-1α, and ALP, in MC3T3-E1 cells. DXM suppressed skeleton ossification in zebrafish and affected bone regeneration in rats with calvarial defects. However, the mineral density of the regenerated bones did not differ significantly between the DXM and control groups. The present study demonstrated that DXM negatively affects the osteogenic function of osteoblasts, leading to impaired skeletal development and bone regeneration. Thus, clinicians should consider the negative effects of DXM on bone regeneration. |
| title | Dextromethorphan Inhibits Osteoblast Differentiation and Bone Regeneration of Rats With Subcritical-Sized Calvarial Defects. |
| topic | Animals Bone Regeneration Osteoblasts Dextromethorphan Cell Differentiation Skull Mice Osteogenesis Rats Zebrafish Cell Line Male Rats, Sprague-Dawley Osteocalcin Core Binding Factor Alpha 1 Subunit |
| url | https://pubmed.ncbi.nlm.nih.gov/39607004/ |