Experimental study on the prevention of bone loss by deferoxamine in type 1 diabetic mice with osteoporosis
10.3760/cma.j.issn.1000-6699.2019.01.012
- VernacularTitle:去铁胺预防1型糖尿病骨丢失的实验研究
- Author:
Dong ZHANG
1
;
Peng ZHAO
;
Jia JIN
;
Xifeng JIANG
;
Honghui SONG
;
Peng JIA
;
Youjia XU
;
Lianfu DENG
Author Information
1. 苏州大学附属第二医院高级病房 215004
- Keywords:
Hypoxia mimicking agent;
Deferoxamine;
Osteoporosis;
Diabete,type 1
- From:
Chinese Journal of Endocrinology and Metabolism
2019;35(1):67-72
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of a hypoxia mimicking agent deferoxamine (DFO) on the mineral density,volume,architecture,strength,and metabolism of the bones in type 1 diabetic mice withosteoporosis.Methods Type 1 diabetic mice model was established by intraperitoneal injections of streptozotocin.The mice were divided into control (normal mice),diabetes mellitus,and DFO groups.Micro-CT was used to analyze the bone mineral density,volume,architecture,and strength of the trabecule in the distal part of femurs.Three point bending test was carried out to evaluate the bone strength.Hematoxylin and eosin (HE) staining was performed to observe the alteration in the number of osteoblasts.Real-time PCR was used to detect the mRNA expressions of Runt-related gene 2 (Runx-2),osteoclacin,and tartrate resistant acid phosphatase (TRAP) in tibias.Western blot was used to detect the protein expressions of Hypoxia-inducible factor-1α(HIF-1α) and vascular endothelial growth factor (VEGF) in tibias.Results There was a decrease in mineral density,volume,strength of bones as well as deteriorated trabecular microarchitecture in diabetic mice as compared to control mice,which were partially improved by DFO treatment.Moreover,DFO treatment increased the number of osteoblasts and mRNA expression levels of Runx-2,osteoclacin,TRAP,as well as protein expression levels of HIF-1 α and VEGF(P＜0.05).Conclusion Bone loss could be partially prevented by DFO treatment in type 1 diabetic osteoporosis mice,which might be ascribed to increased bone formation via stimulating hypoxia inducible factor singnaling pathway.
