Impact of butylparaben on β-cell damage and insulin/PEPCK expression in zebrafish larvae: Protective effects of morin.
Mahima SinghAjay GuruRaman PachaiappanBader O AlmutairiSelvaraj ArokiyarajMuthukaruppan GopiJesu Arockia RajPublished in: Journal of biochemical and molecular toxicology (2023)
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.
Keyphrases
- oxidative stress
- induced apoptosis
- cell cycle arrest
- diabetic rats
- gene expression
- endoplasmic reticulum stress
- aedes aegypti
- poor prognosis
- single cell
- ischemia reperfusion injury
- dna damage
- type diabetes
- cell proliferation
- drosophila melanogaster
- pi k akt
- cell death
- anti inflammatory
- cell therapy
- dna methylation
- long non coding rna
- signaling pathway
- zika virus
- risk assessment
- magnetic resonance imaging
- magnetic resonance
- cardiovascular disease
- binding protein
- heat shock
- cell cycle
- climate change
- bone marrow