Verbascoside attenuates angiotensin-induced hypertension by inhibiting endoplasmic reticulum stress via the Nur77/GFPT2/CHOP pathway

  • Arch Physiol Biochem. 2025 Nov 24:1-19. doi: 10.1080/13813455.2025.2593441.
Kai Liu  1  2 ,  Fansen Meng  1  2 ,  Xiaojian Zhao  1  2
Affiliations
  • 1. Department of Hypertension, Henan Provincial People's Hospital, Zhengzhou City, Henan Province, China.
  • 2. People's Hospital of Zhengzhou University, Zhengzhou City, Henan Province, China.
PMID: 41284022 DOI: 10.1080/13813455.2025.2593441
Abstract

Background: Verbascoside (VB) inhibits endoplasmic reticulum stress (ERS), but its therapeutic potential in hypertension (HTN) is unclear.

Aim: To investigate whether VB inhibits ERS by modulating the Nur77/GFPT2/CHOP axis, thereby ameliorating angiotensin II (Ang II)-induced HTN.

Methods: The cell biological behaviour of HUVECs was determined by CCK-8, LDH kit, scratch assay, and adhesion assay. Oxidative stress factor levels were detected by flow cytometry and kits. The levels of ERS and the Nur77/GFPT2/CHOP pathway-related proteins were examined through Western blot.

Results: VB increased the viability of Ang II-treated HUVECs, inhibited LDH release, and reduced cell migration and adhesion. VB also reduced ERS marker protein levels, while inhibiting oxidative stress and modulating the Nur77/GFPT2/CHOP pathway. VB lowered blood pressure and increased elastic fibre deposition in HTN mice, and Nur77 agonists enhanced the protective impact of VB.

Conclusion: VB hindered Ang II-induced endothelial dysfunction and ERS through modulating the Nur77/GFPT2/CHOP pathway.

Keywords
Nur77/GFPT2/CHOP pathway; Verbascoside; angiotensin II; endoplasmic reticulum stress; hypertension.
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