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Peer-reviewedCC BY-NC-NDBMC musculoskeletal disorders

Effects of azelnidipine, a calcium channel blocker, in a rat femur fracture model.

  • Hilal Kaya1
  • Abdulmecit Albayrak2
  • Ali Aydin3
  • Yasin Bayir4,5
  • Zekai Halici1
5 affiliations
  1. 1Department of Pharmacology, Faculty of Medicine, Atatürk University, Erzurum, 25240, Turkey.
  2. 2Department of Pharmacology, Faculty of Medicine, Atatürk University, Erzurum, 25240, Turkey. [email protected].
  3. 3Department of Orthopaedics, Faculty of Medicine, Atatürk University, Erzurum, 25240, Turkey.
  4. 4Department of Biochemistry, Faculty of Pharmacy, Atatürk University, Erzurum, 25240, Turkey.
  5. 5Department of Pharmacology, Faculty of Medicine, Sakarya University, Sakarya, 54050, Turkey.
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Abstract

Background

Fractures are an important public health problem as they reduce quality of life due to the occurrence of pain and complications. Osteoblasts originate from mesenchymal stem cells and play a vital role in bone formation. They also contain voltage-gated calcium channels. Azelnidipine is a dihydropyridine-derivative blocker of L- and T-type calcium channels. The signalling process involving the L-type calcium channel is important for the function of osteoblasts. Nevertheless, the impact of dihydropyridine chemicals on bone metabolism remains largely unexplored. To the best of our knowledge, no study has yet evaluated the specific effects of azelnidipine on bone healing. The aim of our study was to examine, for the first time, the impact of azelnidipine on the pathophysiology of bone fractures by radiographic and biochemical techniques.Methods

The study included 40 female rats in 5 groups (n = 8 in each group): a healthy sham group, femoral fracture control group, femoral fracture + 4 mg/kg azelnidipine group, femoral fracture + 8 mg/kg azelnidipine group, and femoral fracture + 16 mg/kg azelnidipine group.Results

Serum tumour necrosis factor-α, interleukin-1β, interleukin-17, osteocalcin, osteopontin, total oxidant capacity, and bone-specific alkaline phosphatase levels significantly increased in the fracture control group compared to the sham group (p < 0.05). Azelnidipine treatment significantly reversed these elevations, particularly at the 16 mg/kg dose, restoring TNF-α, IL-1β, IL-17 levels back toward baseline (p < 0.05). Total antioxidant capacity measured in serum decreased in the fracture group 6.47 ± 1.46 U/mL, whereas azelnidipine significantly increased this parameter to 10.01 ± 1.85 U/mL in a dose-dependent manner (p < 0.05). In radiological findings, azelnidipine contributed positively to fracture healing.Conclusion

These results showed that azelnidipine, a calcium channel blocker, exhibits a potential healing effect in this rat femur fracture model, providing the first preclinical evidence of its potential therapeutic utility in bone recovery.

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Cite

BibTeXRIS
BibTeX
@article{kaya2026effects,
  title = {{Effects of azelnidipine, a calcium channel blocker, in a rat femur fracture model.}},
  author = {Hilal Kaya and Abdulmecit Albayrak and Ali Aydin and Yasin Bayir and Zekai Halici},
  journal = {BMC musculoskeletal disorders},
  year = {2026},
  month = jul,
  doi = {10.1186/s12891-026-10269-2},
  url = {https://europepmc.org/article/MED/42902245},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Effects of azelnidipine, a calcium channel blocker, in a rat femur fracture model.
AU  - Hilal Kaya
AU  - Abdulmecit Albayrak
AU  - Ali Aydin
AU  - Yasin Bayir
AU  - Zekai Halici
PY  - 2026
DA  - 2026/07/01
JO  - BMC musculoskeletal disorders
DO  - 10.1186/s12891-026-10269-2
UR  - https://europepmc.org/article/MED/42902245
AB  - Background  Fractures are an important public health problem as they reduce quality of life due to the occurrence of pain and complications. Osteoblasts originate from mesenchymal stem cells and play a vital role in bone formation. They also contain voltage-gated calcium channels. Azelnidipine is a dihydropyridine-derivative blocker of L- and T-type calcium channels. The signalling process involving the L-type calcium channel is important for the function of osteoblasts. Nevertheless, the impact of dihydropyridine chemicals on bone metabolism remains largely unexplored. To the best of our knowledge, no study has yet evaluated the specific effects of azelnidipine on bone healing. The aim of our study was to examine, for the first time, the impact of azelnidipine on the pathophysiology of bone fractures by radiographic and biochemical techniques.Methods  The study included 40 female rats in 5 groups (n = 8 in each group): a healthy sham group, femoral fracture control group, femoral fracture + 4 mg/kg azelnidipine group, femoral fracture + 8 mg/kg azelnidipine group, and femoral fracture + 16 mg/kg azelnidipine group.Results  Serum tumour necrosis factor-α, interleukin-1β, interleukin-17, osteocalcin, osteopontin, total oxidant capacity, and bone-specific alkaline phosphatase levels significantly increased in the fracture control group compared to the sham group (p < 0.05). Azelnidipine treatment significantly reversed these elevations, particularly at the 16 mg/kg dose, restoring TNF-α, IL-1β, IL-17 levels back toward baseline (p < 0.05). Total antioxidant capacity measured in serum decreased in the fracture group 6.47 ± 1.46 U/mL, whereas azelnidipine significantly increased this parameter to 10.01 ± 1.85 U/mL in a dose-dependent manner (p < 0.05). In radiological findings, azelnidipine contributed positively to fracture healing.Conclusion  These results showed that azelnidipine, a calcium channel blocker, exhibits a potential healing effect in this rat femur fracture model, providing the first preclinical evidence of its potential therapeutic utility in bone recovery.
SN  - 1471-2474
ER  -