ArticleFrontiers in pharmacology2024
Protective effect of dexmedetomidine against delayed bone healing caused by morphine via PI3K/Akt mediated Nrf2 antioxidant defense system.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The effects of dexmedetomidine on thiol/disulphide homeostasis in coronary artery bypass surgery: a randomized controlled trial.BMC anesthesiology · 2024Trial
- Melatonin Partially Attenuates Oxycodone-Induced Placental Stress Signaling and Fetal Brain Apoptosis in a Sex-Specific Manner.bioRxiv : the preprint server for biology · 2026Article
- Comparative Molecular Effects of Dexmedetomidine and Propofol on Osteoblast Migration and Osteogenic Gene Expression at Pediatric-Equivalent Concentrations: An In Vitro Study.Current issues in molecular biology · 2026Article
- Alternating Current Stimulation Promotes Healing of Bone Fractures in Rabbits.Bioengineering (Basel, Switzerland) · 2025Article
- Plant essential oil supplementation promotes growth and attenuates lipopolysaccharide (LPS)-induced acute liver injury through SIRT1/PGC-1α signaling pathway in nursery pigs.Animal bioscience · 2025Article
- Evaluating the antimicrobial and anti-inflammatory mechanisms of dexmedetomidine in managing bone infection: a laboratory perspective.BMC musculoskeletal disorders · 2025Article
- Therapeutic Effects and Mechanisms of Icaritin in Parkinson's Disease.Current pharmaceutical design · 2025Review
- Modulation of oxidative stress/NMDA/nitric oxide pathway by topiramate attenuates morphine dependence in mice.Heliyon · 2024Article
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Authors and funding
9 authors.
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Abstract
Background: As a class of analgesics, opioids are frequently used to treat both acute and chronic moderate to severe pain. Patients frequently receive opioid painkillers after orthopedic accidents or surgeries. Evidence suggests that opioid drug users have a 55.1% higher risk of fracture and poor bone repair than non-users of opioid drugs. The key pathogenic alterations in the incidence and progression of poor bone repair are over apoptosis and aging of osteoblasts due to the stress caused by oxidation. Dexmedetomidine (Dex) has been proven to protect against a variety of degenerative illnesses by reducing oxidative stress. However, nothing is known about how it affects bone repair. Methods: PI3K/Akt/Nrf2 pathway was detected by immunofluorescence and Western blot. SOD, CAT, JC-1, dihydroethidium and mitosox were used in the Oxidative Stress. Micro-CT, H&E and Masson's staining, immunohistochemically were performed to evaluate the therapeutic effects of DEX on calvarial defects in the morphine-induced rat model. Results: We found that morphine-induced an imbalance in the metabolism and catabolism of primary rat Osteoblasts. However, these conditions could be inhibited by DEX treatment. In the meantime, DEX induced the expression of Nrf2-regulated antioxidant enzymes such as NQO1, HO-1, GCLm, GCLc, and TrxR1. DEX-mediated Nrf2 activation is linked to the PI3K/Akt signaling system. Furthermore, it has been established that intravenous DEX enhanced the growth of bone healing in a model of a surgically produced rat cranial lesion. Conclusion: This is the first description of the unique DEX mechanism acting as a Nrf2 activator against morphine-mediated oxidative harm, raising the possibility that the substance may be used to prevent bone defects.
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