Curcumin Prevents Diabetic Osteoporosis through Promoting Osteogenesis and Angiogenesis Coupling via NF-κB Signaling

被引:17
作者
Fan, Desheng [1 ]
Lu, Jiuqing [2 ]
Yu, Nijia [2 ]
Xie, Yajia [2 ]
Zhen, Lei [3 ]
机构
[1] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Dept Pathol, Baoshan Branch, Shanghai 201999, Peoples R China
[2] Fudan Univ, Shanghai Stomatol Hosp, Oral Biomed Engn Lab, Shanghai 200001, Peoples R China
[3] Tongji Univ, Tongji Hosp, Sch Med, Dept Stomatol, Shanghai 200065, Peoples R China
关键词
MESENCHYMAL STEM-CELLS; BONE-FORMATION; MINERAL DENSITY; DIFFERENTIATION; APOPTOSIS; RELEASE; MODEL;
D O I
10.1155/2022/4974343
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
Diabetic osteoporosis (DOP) is a metabolic disease which is characterized by impaired bone microarchitecture and reduced bone mineral density resulting from hyperglycemia. Curcumin, an effective component extracted from Curcuma longa, exhibits antioxidation, regulation of bone metabolism and hypoglycemic effects. The BMSC-mediated osteogenesis and angiogenesis coupling seems to be important in bone formation and regeneration. We aimed to explore the effect of curcumin on BMSC-mediated osteogenesis-angiogenesis coupling in high glucose conditions and underlying mechanisms. Our results showed that high glucose impaired the osteogenic and proangiogenic ability of BMSCs and that curcumin pretreatment rescued the BMSC dysfunction induced by high-concentration glucose. Inhibition of the high glucose-activated NF-kappa B signaling pathway has been found to contribute to the protective effects of curcumin on high glucose-inhibited coupling of osteogenesis and angiogenesis in BMSCs. Furthermore, accelerated bone loss and decreased type H vessels were observed in diabetic osteoporosis mice models. However, curcumin treatment prevented bone loss and promoted vessel formation in diabetic osteoporosis mice. Based on these results, we concluded that curcumin ameliorated diabetic osteoporosis by recovering the osteogenesis and angiogenesis coupling of BMSCs in hyperglycemia, partly through inhibiting the high glucose-activated NF-kappa B signaling pathway.
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页数:13
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