Multitarget therapeutic potential of sulforaphane in ethidium bromide-induced neurotoxicity in multiple sclerosis-like pathology: comparison with omaveloxolone and dimethyl fumarate on neuroprotection and systemic recovery.

Authors

Divya Choudhary, Sidharth Mehan, Ritam Mukherjee, Md Nasiruddin Khan, Ghanshyam Das Gupta, Rajaram Samant, Manoj Tongra

Published in

Scientific reports. Jul 09, 2026. Epub Jul 09, 2026.

Abstract

Multiple sclerosis (MS) is a chronic autoimmune disorder characterized by demyelination, neuroinflammation, and neurodegeneration. This study investigates the neuroprotective potential of Sulforaphane (SFN) in ameliorating ethidium bromide (EBRM)-induced MS-like pathology in Wistar rats. The efficacy of SFN at two doses (SFN1.5 and SFN3) was compared to FDA-approved Nrf2 activator drugs, omaveloxolone (OMV15) and dimethyl fumarate (DIMF50). EBRM administration caused neurobehavioral deficits, demyelination, oxidative stress, axonal degeneration, and inflammation. It disrupted key cellular pathways, including Nrf2/HO-1/SIRT-1, JAK/STAT-3/mTOR, and BACE-1/Gamma-secretase/MAPT, as well as caused neurotransmitter imbalances. SFN3 demonstrated significant improvement in motor function, cognitive performance, neurotransmitter levels antioxidant enzymes and alleviated neuroinflammation by modulating inflammatory cytokines. Molecular analyses showed that SFN3 increased Nrf2/HO-1/SIRT-1 levels while decreased pro-inflammatory and neurodegenerative markers such as STAT-3, mTOR, and BACE-1 levels. Gross pathological, Histopathological, and LFB studies indicated reduced demyelination and liver damage. SFN3 also demonstrated favourable systemic safety compared to OMV15. While DIMF50 showed the highest overall efficacy, SFN3 showed consistent modulation of pathological markers, neuroprotective effects, and safety profile. These findings suggest that SFN3 may have therapeutic potential for further translational research in MS. Future studies should validate its clinical relevance and explore combinatorial therapies with existing MS treatments to enhance therapeutic outcomes.

PMID:
42426148
Bibliographic data and abstract were imported from PubMed on 10 Jul 2026.

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