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Vanillic Acid Inhibited the Induced Glycation Using In Vitro and In Vivo Models

Amani Alhadid1, Yasser Bustanji2,3, Amani Harb4

  • 1Department of Pharmacy, Faculty of Pharmacy, Al-Zaytoonah University of Jordan, Amman, Jordan.

Evidence-Based Complementary and Alternative Medicine : Ecam
|November 28, 2022
PubMed
Abstract

Insights

Vanillic acid (VA) demonstrates significant antiglycation properties, effectively reducing advanced glycation end-products (AGEs) in kidney and skin tissues. This natural compound shows promise in combating glycation-related cellular damage.

Area of Science:

  • Biochemistry
  • Pharmacology
  • Cell Biology

Background:

  • Glycation, a process implicated in numerous diseases like diabetes, cancer, neurodegenerative disorders, and aging, involves the non-enzymatic reaction between sugars and proteins.
  • Investigating natural and synthetic compounds for antiglycation activity is crucial for developing therapeutic strategies against glycation-associated pathologies.
  • Vanillic acid (VA), a phenolic compound, was selected for evaluation due to its potential biological activities.

Purpose of the Study:

  • To assess the antiglycation efficacy of vanillic acid (VA) using both in vitro and in vivo experimental models.
  • To determine the cytoprotective effects of VA against methylglyoxal-induced cellular damage.
  • To evaluate the impact of VA on glycation markers in a diabetic rat model.

Main Methods:

  • In vitro antiglycation assay: Bovine serum albumin (BSA) incubated with glucose in the presence of varying concentrations of VA, with aminoguanidine (AMG) as a positive control.
  • Cytoprotective assay: RAW 264.7 cells treated with methylglyoxal and VA, with cell viability assessed using the MTT assay.
  • In vivo study: Streptozotocin-induced diabetic rats treated with different doses of VA for four weeks, measuring serum fructosamine, HbA1c, and detecting advanced glycation end-products (AGEs) in kidney and skin tissues.

Main Results:

  • Vanillic acid exhibited concentration-dependent inhibition of BSA glycation, with an IC50 of 45.53 mM compared to 5.09 mM for AMG.
  • VA significantly enhanced cell viability in a dose-dependent manner when cells were exposed to methylglyoxal.
  • While VA did not alter serum fructosamine or HbA1c levels, it markedly reduced AGEs in the kidneys and skin tissues of diabetic rats.

Conclusions:

  • Vanillic acid possesses significant antiglycation activity, demonstrated through both in vitro assays and in vivo studies.
  • VA provides cytoprotection against glycation-induced cellular damage and reduces the accumulation of advanced glycation end-products.
  • These findings suggest that vanillic acid has potential therapeutic applications in managing diseases associated with long-term glycation.

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