摘要
背景:研究发现,血管内皮生长因子165和骨形态发生蛋白两种因子在缺氧复氧过程中相互作用,通过调节细胞内信号通路的活化,参与骨细胞损伤的修复过程。目的:进一步探究血管内皮生长因子165/骨形态发生蛋白与缺氧复氧成骨细胞损伤的关系分析。方法:取成骨细胞,建立缺氧复氧损伤模型,建模前后Real-Time PCR法和免疫印迹法检测血管内皮生长因子165、骨形态发生蛋白2的mRNA及蛋白表达。分别给予建模后成骨细胞不同质量浓度(10,20,40ng/mL)血管内皮生长因子165或骨形态发生蛋白2处理12,24,36,48,72 h,CCK-8法检测细胞增殖,DAPI检测细胞凋亡。结果与结论:(1)与建模前相比,建模后成骨细胞中血管内皮生长因子165、骨形态发生蛋白2的mRNA和蛋白表达量显著降低(P<0.05);(2)成骨细胞增殖率随着血管内皮生长因子165质量浓度的升高而明显升高(P<0.05);成骨细胞凋亡率随着血管内皮生长因子165质量浓度的升高而明显降低(P<0.05);(3)成骨细胞增殖率随着骨形态发生蛋白2质量浓度的升高而明显升高(P<0.05);成骨细胞凋亡率随着骨形态发生蛋白质量浓度的升高而明显降低(P<0.05);(4)结果表明,血管内皮生长因子165、骨形态发生蛋白在缺氧复氧成骨细胞损伤中低表达,给予血管内皮生长因子165、骨形态发生蛋白处理后缺氧复氧成骨细胞损伤明显降低,且呈浓度依赖性,提示血管内皮生长因子、骨形态发生蛋白对缺氧复氧成骨细胞损伤有明显保护作用。
BACKGROUND:It has been found that vascular endothelial growth factor 165 and bone morphogenetic proteins interact with each other during hypoxiareoxygenation and are involved in the repair process of osteoblast injury by regulating the activation of intracellular signaling pathways.OBJECTIVE:To further investigate the relationship between vascular endothelial growth factor 165/bone morphogenetic protein and hypoxic-reoxygenated osteoblast injury.METHODS:Osteoblasts were selected and the hypoxic-reoxygenated injury model was established.Vascular endothelial growth factor 165 and bone morphogenetic protein expressions at mRNA and protein levels were detected by real-time PCR and western blot before and after modeling.After modeling,osteoblasts were given different concentrations of vascular endothelial growth factor 165 and bone morphogenetic protein 2(10,20,40 ng/mL).Cell proliferation was detected by cell counting kit-8 method and apoptosis was detected by DAPI at 12,24,36,48,and 72 hours after treatment.RESULTS AND CONCLUSION:Compared with before modeling,the mRNA and protein expressions of vascular endothelial growth factor 165 and bone morphogenetic protein 2 in osteoblasts after modeling were significantly decreased(P<0.05).The proliferation rate of osteoblasts was significantly increased with the increase of vascular endothelial growth factor 165 concentration(P<0.05),while the apoptosis rate of osteoblasts decreased significantly with the increase of vascular endothelial growth factor 165 concentration(P<0.05).The proliferation rate of osteoblast was significantly increased with the increase of bone morphogenetic protein 2 concentration(P<0.05),while the apoptosis rate of osteoblast decreased significantly with the increase of bone morphogenetic protein 2 concentration(P<0.05).To conclude,vascular endothelial growth factor 165 and bone morphogenetic protein are lowly expressed in hypoxic-reoxygenated osteoblast injury,and treatment with vascular endothelial growth factor 165 and bone morphogenetic protein can reduce the injury of hypoxic-reoxygenated osteoblast in a concentration-dependent manner,suggesting that vascular endothelial growth factor 165 and bone morphogenetic protein have a significant protective effect against the injury of hypoxic-reoxygenated osteoblasts.
作者
赵伊婷
张裕祥
马洁
何雪娇
Zhao Yiting;Zhang Yuxiang;Ma Jie;He Xuejiao(Department of Orthopedics,The Sixth Affiliated Hospital of Xinjiang Medical University,Urumqi 830001,Xinjiang Uygur Autonomous Region,China;Clinical Laboratory,The Sixth Affiliated Hospital of Xinjiang Medical University,Urumqi 830001,Xinjiang Uygur Autonomous Region,China)
出处
《中国组织工程研究》
CAS
北大核心
2024年第35期5669-5674,共6页
Chinese Journal of Tissue Engineering Research
关键词
血管内皮生长因子165
骨形态发生蛋白2
缺氧复氧
成骨细胞
细胞凋亡
vascular endothelial growth factor 165
bone morphogenetic protein 2
hypoxia-reoxygenation
osteoblast
cell apoptosis
