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Effects of insulin therapy on fracture healing and expression of VEGF in diabetic rats
Da-Wei Wang, Shun-Lei Du, Ming-Tao Xu, Yi-Ting Lu, Zhan-Chao Wang, Le-Xin Wang
Jazyk angličtina Země Česko
Typ dokumentu práce podpořená grantem
NLK
Free Medical Journals
od 2003 do 2013
Freely Accessible Science Journals
od 2003 do 2013
ROAD: Directory of Open Access Scholarly Resources
od 2002
- MeSH
- biomechanika MeSH
- chondrocyty patologie účinky léků MeSH
- experimentální diabetes mellitus farmakoterapie komplikace patofyziologie MeSH
- femur patologie radiografie účinky léků MeSH
- fraktury femuru * farmakoterapie patofyziologie patologie radiografie MeSH
- hojení ran účinky léků MeSH
- imunohistochemie MeSH
- inzulin * terapeutické užití MeSH
- kostní svalek patofyziologie účinky léků MeSH
- modely nemocí na zvířatech MeSH
- potkani Wistar MeSH
- studie případů a kontrol MeSH
- vaskulární endoteliální růstové faktory * analýza účinky léků MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- práce podpořená grantem MeSH
This study was designed to investigate effects of insulin on fracture healing and expression of vascular endothelial growth factor (VEGF) in diabetic rats. Wister rats were randomly divided into diabetic control (n=66), diabetic insulin (=66) and non-diabetic control group (n=66). Diabetes was established by peritoneal injection of alloxan. Tibia fracture was surgically created and was allowed to heal. Radiological and biomechanical examinations were performed on the healing tibia. Immuohistochemistry was used to assess VEGF expression in the healing fracture tissues. Cortical reconstruction of the fracture sites in non-diabetic control and diabetic insulin groups was more rapid than in diabetic control group within 6 weeks of the fracture. Mechanical strength of the affected tibia in the diabetic insulin and non-diabetic control group was superior to diabetic control group. Histological examination of the fracture sites revealed a delay in chondrocyte maturation and hypertrophy in diabetic control group. VEGF expression was widely distributed in fracture sites within the first 4 weeks in control and diabetic insulin treatment group. However VEGF expression in the callus and periosteum in diabetic control group was much less than in diabetic insulin or non-diabetic control group. In conclusion, diabetes delays fracture healing and adversely affects callus formation with a reduced VEGF expression at the fracture sites. Insulin therapy improves fracture healing in diabetes rats, possibly through enhancing VEGF expression in the fractured bones.
Citace poskytuje Crossref.org
Literatura
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- $a Wang, Da-Wei $u Department of Orthopedic Surgery, Liaocheng People's Hospital and Liaocheng Clinical School of Taishan Medical University, Liaocheng, China; School of Biomedical Sciences, Charles Sturt University, Wagga Wagga, Australia
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- $a This study was designed to investigate effects of insulin on fracture healing and expression of vascular endothelial growth factor (VEGF) in diabetic rats. Wister rats were randomly divided into diabetic control (n=66), diabetic insulin (=66) and non-diabetic control group (n=66). Diabetes was established by peritoneal injection of alloxan. Tibia fracture was surgically created and was allowed to heal. Radiological and biomechanical examinations were performed on the healing tibia. Immuohistochemistry was used to assess VEGF expression in the healing fracture tissues. Cortical reconstruction of the fracture sites in non-diabetic control and diabetic insulin groups was more rapid than in diabetic control group within 6 weeks of the fracture. Mechanical strength of the affected tibia in the diabetic insulin and non-diabetic control group was superior to diabetic control group. Histological examination of the fracture sites revealed a delay in chondrocyte maturation and hypertrophy in diabetic control group. VEGF expression was widely distributed in fracture sites within the first 4 weeks in control and diabetic insulin treatment group. However VEGF expression in the callus and periosteum in diabetic control group was much less than in diabetic insulin or non-diabetic control group. In conclusion, diabetes delays fracture healing and adversely affects callus formation with a reduced VEGF expression at the fracture sites. Insulin therapy improves fracture healing in diabetes rats, possibly through enhancing VEGF expression in the fractured bones.
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