Impact of butylparaben on β‐cell damage and insulin/PEPCK expression in zebrafish larvae: Protective effects of morin

Author:

Singh Mahima1,Guru Ajay2ORCID,Pachaiappan Raman1,Almutairi Bader O.3,Arokiyaraj Selvaraj4,Gopi Muthukaruppan1,Arockiaraj Jesu5ORCID

Affiliation:

1. Department of Biotechnology School of Bioengineering, Faculty of Engineering and Technology, SRM Institute of Science and Technology Kattankulathur Tamil Nadu India

2. Department of Cariology Saveetha Dental College and Hospitals, SIMATS Chennai Tamil Nadu India

3. Department of Zoology College of Science, King Saud University Riyadh Saudi Arabia

4. Department of Food Science & Biotechnology Sejong University Seoul South Korea

5. Toxicology and Pharmacology Laboratory, Department of Biotechnology Faculty of Science and Humanities, SRM Institute of Science and Technology Kattankulatur Tamil Nadu India

Abstract

AbstractButylparaben (BP), a common chemical preservative in cosmetic and pharmaceutical products, has been known to induce oxidative stress and disrupt endocrine function in humans. In contrast, morin, a flavonoid derived from the Moraceae family, exhibits diverse pharmacological properties, including anti‐inflammatory and antioxidant. Despite this, the protective role of morin against oxidative stress‐induced damage in pancreatic islets remains unclear. Therefore, in this study, we aimed to investigate the potential protective mechanism of morin against oxidative stress‐induced damage caused by BP in zebrafish larvae. To achieve this, we exposed the zebrafish larvae to butylparaben (2.5 mg/L) for 5 days, leading to increased oxidative stress and apoptosis in β‐cells. However, our compelling findings revealed that pretreatment with various concentrations of morin effectively reduced mortality and mitigated apoptosis and lipid peroxidation in β‐cells induced by BP exposure. In addition, zebrafish larvae exposed to BP for 5 days exhibited evident β‐cell damage. However, the pretreatment with morin showed promising effects by promoting β‐cell proliferation and lowering glucose levels. Furthermore, gene expression studies indicated that morin pretreatment normalized PEPCK expression while increasing insulin expression in BP‐exposed larvae. In conclusion, our findings highlight the potential of morin as a protective agent against BP‐induced β‐cell damage in zebrafish larvae. The observed improvements in oxidative stress, apoptosis, and gene expression patterns support the notion that morin could be further explored as a therapeutic candidate to counteract the detrimental effects of BP exposure on pancreatic β‐cells.

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Toxicology,Molecular Biology,Molecular Medicine,Biochemistry,General Medicine

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