Catalpol regulates apoptosis and proliferation of endothelial cell via activating HIF-1α/VEGF signaling pathway

Sci Rep. 2024 Nov 16;14(1):28327. doi: 10.1038/s41598-024-78126-7.

Abstract

Burn injuries, especially severe ones, causes microcirculation disorders in local wounds and distant tissues, leading to ischemia and hypoxia of body tissues and organs. The key to prevent and treat complications and improve prognosis after burns is to improve the state of ischemia and hypoxia of tissue and restore the blood supply of organs. Catalpol is an iridoid glycoside compound isolated from Rehmannia radix, which has been widely reported to have various of functions, including antioxidative stress, anti-inflammation, anti-apoptosis, and neuroprotection. However, the pharmacologic action and underlying mechanism of Catalpol in angiogenesis after burn injury remains unclear. The study investigated whether Catalpol regulates apoptosis and proliferation following vascular injury induced by burns using an in vitro model of oxygen-glucose deprivation (OGD) with a human umbilical vein endothelial (HUVE) cell line. The results showed that treatment with Catalpol reduces the level of apoptosis and promotes proliferation of endothelial cell. Mechanistically, Catalpol increases the expression of vascular endothelial growth factor (VEGF) by activating Hypoxia-inducible factor-1α (Hif-1α), resulting in increased expression of related downstream effector molecules. The current study suggested that Catalpol is a promising compound for endothelial protection in burns. It may be an efficient Hif-1α activator for endothelial cell deprived of oxygen and glucose.

Keywords: Apoptosis; Catalpol; Endothelial cell; Hif-1α; Proliferation; VEGF.

MeSH terms

  • Apoptosis* / drug effects
  • Burns / drug therapy
  • Burns / metabolism
  • Burns / pathology
  • Cell Proliferation* / drug effects
  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism
  • Glucose / metabolism
  • Human Umbilical Vein Endothelial Cells* / drug effects
  • Human Umbilical Vein Endothelial Cells* / metabolism
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit* / metabolism
  • Iridoid Glucosides* / pharmacology
  • Signal Transduction* / drug effects
  • Vascular Endothelial Growth Factor A* / metabolism

Substances

  • catalpol
  • Iridoid Glucosides
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Vascular Endothelial Growth Factor A
  • HIF1A protein, human
  • VEGFA protein, human
  • Glucose