# Azelaic acid reduces arsenic-induced toxicity and inflammation in the rat islets of langerhans

**Authors:** Sara Mostafalou, Fatemeh Moafi-Madani, Maryam Baeeri, Mahban Rahimifard, Hamed Haghi-Aminjan

PMC · DOI: 10.22038/ijbms.2025.84651.18311 · 2025-01-01

## TL;DR

Azelaic acid helps protect rat pancreatic islets from arsenic-induced damage by reducing toxicity and inflammation.

## Contribution

This study demonstrates azelaic acid's protective effects against arsenic toxicity in pancreatic islets for the first time.

## Key findings

- Sodium arsenite reduced cell viability and increased apoptosis, ROS, and inflammation in islets.
- Azelaic acid significantly reversed the harmful effects of sodium arsenite on islet cells.
- Azelaic acid's protective role is linked to its anti-apoptotic, anti-inflammatory, and antioxidant properties.

## Abstract

Arsenic is classified as a toxic metal that is naturally found in the Earth’s crust, and long-term exposure to it can result in chronic human disorders like cancer and diabetes. Azelaic acid (AZA), a natural dicarboxylic acid, has been reported to have anti-oxidant and anti-inflammatory effects; hence, it may protect against the metabolic toxicity of arsenic. This study aimed to investigate whether AZA could ameliorate sodium arsenite (SA) toxicity toward rat islets of Langerhans.

Pancreatic Islets of Langerhans isolated from adult male Wistar rats were divided into four groups of 10: control, SA, AZA, and SA plus AZA. Twenty-four hours after incubation, cell viability, cell death pathways, reactive oxygen species (ROS), inflammatory factor gene expression, and insulin secretion were evaluated.

SA dose-dependently decreased cell viability, increased apoptosis, ROS generation, expression of inflammatory mediators (NF-κB, IL-1β, and TNF-α), and insulin secretion. AZA was able to ameliorate all these changes significantly.

Our results indicate that SA can potentially disrupt cellular homeostasis and function in the islets of Langerhans and can increase the risk of metabolic diseases such as diabetes. On the other hand, AZA protected islets of Langerhans against the toxic effects of SA, seemingly due to its anti-apoptotic, anti-inflammatory, and anti-oxidant properties, indicating that AZA may have the potential to run intracellular mechanisms beneficial for coping with the metabolic toxicity of arsenic.

## Linked entities

- **Genes:** NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790], IL1B (interleukin 1 beta) [NCBI Gene 3553], TNF (tumor necrosis factor) [NCBI Gene 7124]
- **Chemicals:** arsenic (PubChem CID 5359596), azelaic acid (PubChem CID 2266), sodium arsenite (PubChem CID 443495)
- **Diseases:** diabetes (MONDO:0005015)
- **Species:** Rattus norvegicus (taxon 10116)

## Full-text entities

- **Genes:** Tnf (tumor necrosis factor) [NCBI Gene 24835] {aka RATTNF, TNF-alpha, Tnfa}, Il1b (interleukin 1 beta) [NCBI Gene 24494] {aka IL-1F2}
- **Diseases:** diabetes (MESH:D003920), toxicity (MESH:D064420), metabolic diseases (MESH:D008659), cancer (MESH:D009369), inflammation (MESH:D007249)
- **Chemicals:** SA (MESH:C017947), AZA (MESH:C010038), Arsenic (MESH:D001151), dicarboxylic acid (MESH:D003998), ROS (MESH:D017382)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12057746/full.md

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Source: https://tomesphere.com/paper/PMC12057746