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还原型 H 血管与去负荷诱导的骨丢失的偶联及西洋参总皂苷在雄性小鼠中的保护作用。

The coupling of reduced type H vessels with unloading-induced bone loss and the protection role of Panax quinquefolium saponin in the male mice.

机构信息

Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China; State Key Lab of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center, Beijing, China; Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China.

State Key Lab of Space Medicine Fundamentals and Application, China Astronaut Research and Training Center, Beijing, China.

出版信息

Bone. 2021 Feb;143:115712. doi: 10.1016/j.bone.2020.115712. Epub 2020 Oct 24.

DOI:10.1016/j.bone.2020.115712
PMID:33164873
Abstract

Unloading-induced bone loss is a critical complication characterized by the imbalance of bone formation and resorption induced by long-term confinement in bed or spaceflight. CD31Emcn (type H) vessel is a specific subtype of capillary, which was coupled with osteogenesis. However, the change of type H vessel and its contributions to the unloading-induced bone loss remains undisclosed. Herein, we found that bone formation and the number of type H vessels were synchronously reduced in the hindlimb-unloading (HU) mice. Panax quinquefolium saponin (PQS) could increase bone mass, osteoblast function and the number of type H vessels in the HU mice. In vitro, PQS treatment accelerated HMECs migration, augmented the total tube loops and increased the secretion of VEGF and Noggin. Primary osteoblasts function was obviously increased when treated with supernatant from PQS-treated HMECs. These effects of PQS were substantially counteracted when VEGF and Noggin in HMECs were knocked down by siRNA. These results demonstrated that unloading-induced bone loss is coupled with reduction of type H vessels and PQS performs preventive function via promoting type H vessel angiogenesis, which is closely associated with endothelial cell-derived VEGF and Noggin.

摘要

去负荷导致的骨丢失是一种严重的并发症,其特征是长期卧床或太空飞行引起的骨形成和吸收失衡。CD31Emcn(H 型)血管是毛细血管的一种特殊亚型,与成骨作用相关。然而,H 型血管的变化及其对去负荷诱导的骨丢失的影响仍未被揭示。在此,我们发现下肢去负荷(HU)小鼠的骨形成和 H 型血管数量同步减少。西洋参总皂苷(PQS)可增加 HU 小鼠的骨量、成骨细胞功能和 H 型血管数量。在体外,PQS 处理可促进 HMECs 的迁移,增加总管环数,并增加 VEGF 和 Noggin 的分泌。当用 PQS 处理的 HMECs 的上清液处理时,原代成骨细胞的功能明显增加。当用 siRNA 敲低 HMECs 中的 VEGF 和 Noggin 时,PQS 的这些作用会显著抵消。这些结果表明,去负荷导致的骨丢失与 H 型血管的减少有关,PQS 通过促进 H 型血管生成发挥预防作用,这与内皮细胞衍生的 VEGF 和 Noggin 密切相关。

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