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吡咯喹啉醌通过抑制氧化应激影响去势雌鼠骨折愈合过程的机制。

The mechanism of pyrroloquinoline quinone influencing the fracture healing process of estrogen-deficient mice by inhibiting oxidative stress.

机构信息

Department of Orthopedics, Zhong Da Hospital, School of Medicine, Southeast University, Nanjing 210009, Jiangsu, China.

The Research Center for Bone and Stem Cells, Nanjing Medical University, Nanjing 211166, Jiangsu, China.

出版信息

Biomed Pharmacother. 2021 Jul;139:111598. doi: 10.1016/j.biopha.2021.111598. Epub 2021 Apr 23.

DOI:10.1016/j.biopha.2021.111598
PMID:33895522
Abstract

It is reported that oxidative stress plays a detrimental role in the process of bone fracture healing. And pyrroloquinoline quinone (PQQ) is used as antioxidant. However, there is no report about whether PQQ supplementation can promote fracture healing by eliminating oxidative stress. To investigate the protective effect of PQQ on fracture healing, open mid-diaphyseal femur fractures model were created in sham, ovariectomized (OVX) mice and PQQ-treated OVX mice. Our results confirmed that PQQ played a preventive and protective role in OVX-induced delay of bone fracture healing by inhibiting oxidative stress, subsequently promoting osteoblastic bone formation and inhibiting osteoclastic bone resorption. The findings of this study not only revealed the mechanism of PQQ supplementation in promoting fracture healing, but also provide experimental and theoretical basis for the clinical application of PQQ in the treatment of bone fracture.

摘要

据报道,氧化应激在骨折愈合过程中起有害作用。吡咯并喹啉醌(PQQ)可用作抗氧化剂。然而,目前尚无关于 PQQ 补充剂是否可以通过消除氧化应激来促进骨折愈合的报道。为了研究 PQQ 对骨折愈合的保护作用,我们在假手术、去卵巢(OVX)小鼠和 PQQ 处理的 OVX 小鼠中创建了开放性骨干骨折模型。我们的结果证实,PQQ 通过抑制氧化应激在 OVX 诱导的骨骨折愈合延迟中发挥预防和保护作用,从而促进成骨细胞的骨形成并抑制破骨细胞的骨吸收。本研究的结果不仅揭示了 PQQ 补充剂促进骨折愈合的机制,而且为 PQQ 在治疗骨折中的临床应用提供了实验和理论基础。

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