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姜黄素通过NF-κB信号通路促进成骨与血管生成偶联来预防糖尿病性骨质疏松症。

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

作者信息

Fan Desheng, Lu Jiuqing, Yu Nijia, Xie Yajia, Zhen Lei

机构信息

Department of Pathology, Baoshan Branch, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 201999, China.

Oral Biomedical Engineering Laboratory, Shanghai Stomatological Hospital, Fudan University, Shanghai 200001, China.

出版信息

Evid Based Complement Alternat Med. 2022 Nov 7;2022:4974343. doi: 10.1155/2022/4974343. eCollection 2022.

Abstract

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 , 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-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-B signaling pathway.

摘要

糖尿病性骨质疏松症(DOP)是一种代谢性疾病,其特征在于骨微结构受损以及高血糖导致的骨矿物质密度降低。姜黄素是从姜黄中提取的一种有效成分,具有抗氧化、调节骨代谢和降血糖作用。骨髓间充质干细胞(BMSC)介导的成骨与血管生成偶联在骨形成和再生中似乎很重要。我们旨在探讨姜黄素在高糖条件下对BMSC介导的成骨-血管生成偶联的影响及其潜在机制。我们的结果表明,高糖损害了BMSCs的成骨和促血管生成能力,而姜黄素预处理可挽救高浓度葡萄糖诱导的BMSC功能障碍。已发现抑制高糖激活的NF-κB信号通路有助于姜黄素对高糖抑制的BMSCs成骨与血管生成偶联的保护作用。此外,在糖尿病性骨质疏松症小鼠模型中观察到骨质流失加速和H型血管减少。然而,姜黄素治疗可预防糖尿病性骨质疏松症小鼠的骨质流失并促进血管形成。基于这些结果,我们得出结论,姜黄素通过恢复高血糖状态下BMSCs的成骨与血管生成偶联来改善糖尿病性骨质疏松症,部分是通过抑制高糖激活的NF-κB信号通路实现的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c8d4/9663221/b896e38620ab/ECAM2022-4974343.001.jpg

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