CORONARY ARTERY DISEASE / RESEARCH PAPER
 
KEYWORDS
TOPICS
ABSTRACT
Introduction:
The aim of this study was to investigate the effects of glabridin on vascular inflammation and vascular remodeling of the left anterior descending artery (LAD) in diabetic rat heart.

Material and methods:
Eighty male Wistar rats were divided into five groups: (1) control rats; (2) glabridin control rats that received diet supplemented with glabridin (CGB); (3) diabetic rats (STZ); (4) diabetic rats that received a supplemented with glabridin (STZ + GB) 40 mg/kg BW; and (5) diabetic rats treated with glyburide (STZ + GR) 4 mg/kg BW. Diabetic animals were rendered diabetic by injection of a single dose (60 mg/kg BW) of streptozotocin (STZ). After 8 weeks, the biochemical markers of oxidative stress were assessed. The three-dimensional morphology of LAD was examined by vascular corrosion casting. Enzyme-linked immunosorbent assay was applied to determine the expression of TNF-α and IL-1β proteins. Western blot and immunofluorescence analysis were used to detect the expression of VEGF and TGF-β1 secretions.

Results:
The lumen diameter of the LAD was notably smaller and stenotic. LAD analysis revealed arterial notch and evolved irregular caliber. Moreover, neovascularization appeared and was extensive. The Trolox equivalent antioxidant capacities and Trolox equivalent antioxidant capacity levels of heart tissue were significantly decreased and levels of malondialdehyde were found to be elevated in STZ rats whereas they were improved in the STZ + GB group. Increased expression levels of VEGF, TGF-β1, TNF-α, and IL-1β proteins in heart tissues were observed in the STZ group. The inflammation cytokine levels were decreased in the STZ + GB group.

Conclusions:
These results revealed that glabridin was able to reduce LAD and heart tissue damage. Glabridin can be an antioxidant and can reduce the pathology of the LAD in terms of reducing inflammation and restoring condition of the LAD. It would be beneficial in examining the role of glabridin as a therapeutic aim in diabetes treatment research in coronary artery disease.

eISSN:1896-9151
ISSN:1734-1922