Vitamin B-2 Prevents Glucocorticoid-Caused Damage of Blood Vessels in Osteonecrosis of the Femoral Head

作者全名："Guo, MinKang; Zhang, Jian"

作者地址："[Guo, MinKang; Zhang, Jian] Chongqing Med Univ, Orthoped Lab, Chongqing, Peoples R China; [Guo, MinKang; Zhang, Jian] Chongqing Med Univ, Affiliated Hosp 1, Dept Orthoped, Chongqing, Peoples R China"

通信作者："Zhang, J (通讯作者)，Chongqing Med Univ, Orthoped Lab, Chongqing, Peoples R China.; Zhang, J (通讯作者)，Chongqing Med Univ, Affiliated Hosp 1, Dept Orthoped, Chongqing, Peoples R China."

来源：BIOMED RESEARCH INTERNATIONAL

ESI学科分类：BIOLOGY & BIOCHEMISTRY

WOS号：WOS:000831625200014

JCR分区：Q3

影响因子：3.246

年份：2022

卷号：2022

期号：　

开始页：　

结束页：　

文献类型：Article

关键词：　

摘要："Osteonecrosis of the femoral head (ONFH) is a disorder that can cause collapse of the femoral head. The damage and dysfunction of femoral head microvascular endothelial cells are related to the pathogenesis of glucocorticoid-induced ONFH. Reports suggest that vitamin B-2 can promote osteoblast differentiation and prevent low bone mineral density and prevent reperfusion oxidative injury. To explore the effect and possible molecular mechanism of vitamin B-2 on the ONFH and Human Umbilical Vein Endothelial Cells (HUVECs), we performed a rat model of ONFH by dexamethasone. The rats were randomly divided into four groups: control group, vitamin B-2 group, dexamethasone group, and dexamethasone combined with vitamin B-2 treatment group. HUVECs were used to further prove the role and mechanism of vitamin B-2 in vitro. In patients, according to immunohistochemical and qRT-PCR of the femoral head, the angiogenic capacity of the ONFH femoral head is compromised. In vivo, it showed that vitamin B-2 could inhibit glucocorticoid-induced ONFH-like changes in rats by suppressing cell apoptosis, promoting the regeneration of blood vessels, and increasing bone mass. According to in vitro results, vitamin B-2 could induce the migration of HUVECs, enhance the expression of angiogenesis-related factors, and inhibit glucocorticoid-induced apoptosis. The underlying mechanism may be that vitamin B-2 activates the PI3K signaling pathway. Vitamin B-2 alleviated dexamethasone-induced ONFH, and vitamin B-2 could promote the proliferation and migration of HUVECs and inhibit their apoptosis by activating the PI3K/Akt signaling pathway. Vitamin B-2 may be a potentially effective treatment for ONFH."

基金机构：Orthopedics Department of the First Affiliated Hospital of Chongqing Medical University; General Project of Technology Innovation Application Development of Chongqing Science and Technology Bureau [cstc2019jscx-msxmX0245]

基金资助正文：AcknowledgmentsThis study was performed with the help of the Orthopedics Department of the First Affiliated Hospital of Chongqing Medical University. This work was supported by the General Project of Technology Innovation Application Development of Chongqing Science and Technology Bureau (Grant No. cstc2019jscx-msxmX0245).