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

莫林 斑马鱼 药理学 化学 生物 医学 生物化学 病理 基因
作者
Mahima Singh,Ajay Guru,Raman Pachaiappan,Bader O. Almutairi,Selvaraj Arokiyaraj,Muthukaruppan Gopi,Jesu Arockiaraj
出处
期刊:Journal of Biochemical and Molecular Toxicology [Wiley]
卷期号:38 (1) 被引量:3
标识
DOI:10.1002/jbt.23520
摘要

Abstract Butylparaben (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.
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