Abstract
The extended exposure to inorganic arsenic is commonly linked to brain damage through oxidative and apoptotic processes. The compound known as Garcinol (GCL) has garnered significant interest due to its potential advantages for human well-being. Nevertheless, the ability of GCL to protect against toxicity generated by arsenic in the brain has not yet been investigated. Hence, our study aimed to examine the neuroprotective effectiveness of GCL in mitigating the detrimental impacts of sodium arsenite (SA) on behavioral patterns, the molecular mechanisms, apoptotic markers, and oxidative stress parameters in the brain, liver, and kidney of mice. The mice were categorized into four distinct groups for the duration of 28 days: Group I, referred to as the Control group, received a 5% v/v solution of DMSO; Group II, referred to as the SA group, received a dosage of 20 mg/kg of SA; Group III, referred to as the SA+GCL group, received a combined dosage of 20 mg/kg of SA and 50 mg/kg of GCL; and Group IV, referred to as the GCL group, received a dosage of 50 mg/kg of GCL. Following the administration of the drug, an evaluation was conducted to analyze the behavior of the animals. Additionally, the levels of AchE, ATP hydrolysis, and angiotensin I-converting enzyme (ACE), which are known to be associated with cognitive function, were examined. The findings of our study demonstrated that the administration of GCL led to enhancements in cognitive behavior. Additionally, GCL was found to mitigate the cholinergic deficit, as evidenced by the reduction of acetylcholinesterase (AchE) activity. Furthermore, GCL was observed to increase the signaling of glycogen synthase kinase 3 beta (GSK3β) and cAMP response elementbinding protein (CREB) in mice treated with SA. In addition, it was observed that GCL exhibited an enhancement in redox equilibrium and provided defense against oxidative harm generated by SA in the brains of mice. This effect was mediated through the activation of NRF2/HO-1 proteins and resulted in a noteworthy decrease in malondialdehyde concentrations. Thus, treatment with GCL ameliorated neurobehavior, modulated cognitive function-associated biomarkers, and protected mice from SA-induced neurotoxicity, according to the findings of this pre clinical study.
Recommended Citation
Algefare, Abdulmohsen I.
(2025)
"Effect of garcinol against arsenic-induced neurobehavioral alterations and liver and kidney dysfunction in albino mice,"
BioMedicine: Vol. 15
:
Iss.
3
, Article 4.
DOI: 10.37796/2211-8039.1650
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