Terminalia chebula Fruit Extract Ameliorates Peripheral Edema by Inhibiting NF-κB and MAPK Signaling Pathways.

Area of Science:

• Pharmacology
• Molecular Biology
• Pathology

Background:

• Peripheral edema stems from fluid buildup due to increased vascular permeability and inflammation.
• Understanding the molecular basis of edema is crucial for developing effective treatments.

Purpose of the Study:

• To evaluate the therapeutic potential of Terminalia chebula extract (TCE) in managing inflammation-induced peripheral edema.
• To elucidate the molecular mechanisms underlying TCE's anti-edema effects.

Main Methods:

• In vitro: Assessed TCE's impact on human umbilical vein endothelial cells (HUVECs) for viability, inflammatory gene expression, reactive oxygen species (ROS), barrier integrity, and vascular endothelial growth factor (VEGF)-induced migration.
• In vivo: Utilized acetic acid-induced peritoneal vascular permeability and carrageenan-induced paw edema models in rodents.
• Analyzed NF-κB and MAPK signaling pathways, performed histological examinations, and measured serum TNF-α levels.

Main Results:

• TCE significantly improved HUVEC viability, reduced inflammatory gene expression (TNF, IL6, PTGS2), and decreased ROS levels.
• TCE enhanced endothelial barrier integrity, increased transendothelial electrical resistance, and inhibited VEGF-induced migration.
• In vivo studies showed TCE significantly reduced vascular permeability and paw edema, with decreased inflammatory markers and improved histology.

Conclusions:

• TCE attenuates peripheral edema by preserving endothelial barrier function and suppressing key inflammatory signaling pathways (NF-κB, MAPK).
• These findings support TCE's potential as a therapeutic agent for vascular dysfunction and edema associated with inflammation.