Sulforaphane (4-methylsulfnylbutyl isothiocyanate) mitigates gold nanoparticle induced brain toxicity in male albino rats

Abstract

ObjectiveGold nanoparticles (GNPs) have shown great promise for a variety of biomedical applications; however, emerging evidence suggests that they exhibit toxic effects on different organs including the brain. Sulforaphane (SFN) is a naturally occurring compound derived from plants, which has been recognized for its impressive antioxidant, anticancer, and anti-inflammatory characteristics. The neuroprotective potential of SFN was assessed in this study to determine its effectiveness against GNP-induced toxicity in brain tissues. MethodsMale Wistar rats were administered GNPs daily, either alone or in combination with SFN, over a 7-day period. Inflammatory and oxidative stress markers including serotonin and Nrf2 levels were measured in brain tissues. Histological changes were assessed for GNP-mediated tissue damage. ResultsCompared with the control, GNP-treated rats exhibited a significant increase in brain inflammatory and oxidative stress (OS) markers including MDA, 8OHdG, and IL-6 and a significant decrease in Glutathione S-transferase, Glutathione reductase, SOD, Total antioxidant capacity, Nrf2, brain parameters (serotonin, dopamine, Gama Amino Butyric Acid) and Brain-derived neurotrophic factor. GNP treatment also resulted in marked histopathological changes in brain tissue. In addition, rats administered with combined GNP and SFN showed a significant reversal in the levels of these biomarkers. SFN also protected brain tissue from GNP-induced histopathological changes Molecular docking studies confirmed the competitive binding of SFN with GNPs to amino acid receptor proteins, 1MAH and 1KU6, which supports the experimental data. ConclusionCollectively, our findings indicate the neuroprotective capacity of SFN against GNP-induced brain damage, presumably by blocking OS and inflammation.