Abstract
The objective of this study was to quantify pentagalloyl glucose (PGG) mediated biomechanical restoration of degenerated extracellular matrix (ECM). Planar biaxial tensile testing was performed for native (N), enzyme-treated (collagenase and elastase) (E), and PGG (P) treated porcine abdominal aorta specimens (n = 6 per group). An Ogden material model was fitted to the stress–strain data and finite element computational analyses of simulated native aorta and aneurysmal abdominal aorta were performed. The maximum tensile stress of the N group was higher than that in both E and P groups for both circumferential (43.78 ± 14.18 kPa vs. 10.03 ± 2.68 kPa vs. 13.85 ± 3.02 kPa; p = 0.0226) and longitudinal directions (33.89 ± 8.98 kPa vs. 9.04 ± 2.68 kPa vs. 14.69 ± 5.88 kPa; p = 0.0441). Tensile moduli in the circumferential direction was found to be in descending order as N > P > E (195.6 ± 58.72 kPa > 81.8 ± 22.76 kPa > 46.51 ± 15.04 kPa; p = 0.0314), whereas no significant differences were found in the longitudinal direction (p = 0.1607). PGG binds to the hydrophobic core of arterial tissues and the crosslinking of ECM fibers is one of the possible explanations for the recovery of biomechanical properties observed in this study. PGG is a beneficial polyphenol that can be potentially translated to clinical practice for preventing rupture of the aneurysmal arterial wall.
Highlights
The etiology of abdominal aortic aneurysm (AAA) development is believed to be multi-factorial, in that (i) the pathology is initiated at the molecular level; (ii) it builds up to the tissue level through extracellular matrix (ECM) and structural changes; and (iii) it manifests as geometrical, biomechanical, and blood flow-related alterations in the abdominal aorta, resulting in rupture if left untreated [1,2,3]
We report on the ability of pentagalloyl glucose (PGG) to restore the biomechanical properties of the porcine abdominal aorta after enzymatic damage
A PGG-based treatment would be aimed at preventing the progressive increase in aneurysm size and the eventual rupture of the abdominal aorta
Summary
The etiology of abdominal aortic aneurysm (AAA) development is believed to be multi-factorial, in that (i) the pathology is initiated at the molecular level (protease- and enzyme-related); (ii) it builds up to the tissue level through extracellular matrix (ECM) and structural changes; and (iii) it manifests as geometrical-, biomechanical-, and blood flow-related alterations in the abdominal aorta, resulting in rupture if left untreated [1,2,3]. Most aneurysms exhibit an intraluminal thrombus (ILT), which is a source of proteolytic activity [9], increased wall weakening [10], and a preferential site for rupture [11]. This multifaceted presentation of the disease makes the discovery of potential pharmacological targets a complex one (i.e., it has to consider the biological factors, the biomechanical environment, and the presence of ILT as a potential transport barrier)
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