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Objective <p>To explore the mechanism of glycosides from BYHWD promote EPCs repairing damaged vascular endothelium.</p> Methods <p>A model of vascular intimal damage in rats and an aging model in EPCs were established. HE staining was carried out to examine the blood vessel intima; Elisa assays were employed to assess the levels of TC, TG, HDL-C, LDL-C, Col-1, MMP-9, and TIMP-1; frozen sections were utilized to detect the homing status of EPCs in vivo; western blot was used to detect the contents of eNOS, ITGβ3, ITGβ6, FAK, P-FAK, ERK1/2 and P-ERK1/2; the CCK-8 assay was used to evaluate the proliferation rate; the cell migration test was used to evaluate cell migration capabilities; and the tube formation test was used to determine the tube formation ability.</p> Results <p>BYHWD, glycosides, and EPCs are capable of ameliorating intimal thickening. They can increase the levels of eNOS, raise HDL levels, and reduce TG, TC, and LDL levels. Moreover, glycosides can promote the function of EPCs following vascular intimal damage. BYHWD and glycosides can decrease the rate of EPCs cell aging and increase the cell proliferation rate, migration ability, and tube-forming function in the aging model. BYHWD and glycosides can down regulate P-FAK, P-ERK, ITGβ3, ITGβ6, Col-1, and MMP-9, while up regulate TIMP-1 levels in the aging model. Additionally, glycosides can promote EPCs to change the levels of these proteins.</p> Conclusion <p>Glycosides promote EPC-mediated repair of damaged vascular endothelium through inhibiting the integrin/ECM via FAK/ERK pathway.</p> Graphical Abstract <p></p>

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A novel mechanistic insight: BYHWD glycosides promote vascular endothelial repair via EPCs

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月24日

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  • Fan-Chen Yan,
  • Zheng-Ji Sun,
  • Wei Tan,
  • Lu Ma,
  • Xiao-Dan Liu,
  • Huang Ding,
  • Wei Zhang

摘要

Objective

To explore the mechanism of glycosides from BYHWD promote EPCs repairing damaged vascular endothelium.

Methods

A model of vascular intimal damage in rats and an aging model in EPCs were established. HE staining was carried out to examine the blood vessel intima; Elisa assays were employed to assess the levels of TC, TG, HDL-C, LDL-C, Col-1, MMP-9, and TIMP-1; frozen sections were utilized to detect the homing status of EPCs in vivo; western blot was used to detect the contents of eNOS, ITGβ3, ITGβ6, FAK, P-FAK, ERK1/2 and P-ERK1/2; the CCK-8 assay was used to evaluate the proliferation rate; the cell migration test was used to evaluate cell migration capabilities; and the tube formation test was used to determine the tube formation ability.

Results

BYHWD, glycosides, and EPCs are capable of ameliorating intimal thickening. They can increase the levels of eNOS, raise HDL levels, and reduce TG, TC, and LDL levels. Moreover, glycosides can promote the function of EPCs following vascular intimal damage. BYHWD and glycosides can decrease the rate of EPCs cell aging and increase the cell proliferation rate, migration ability, and tube-forming function in the aging model. BYHWD and glycosides can down regulate P-FAK, P-ERK, ITGβ3, ITGβ6, Col-1, and MMP-9, while up regulate TIMP-1 levels in the aging model. Additionally, glycosides can promote EPCs to change the levels of these proteins.

Conclusion

Glycosides promote EPC-mediated repair of damaged vascular endothelium through inhibiting the integrin/ECM via FAK/ERK pathway.

Graphical Abstract