The Journal of pharmacy and pharmacology · 2026
Naringenin confers neuroprotection in a cuprizone-induced mouse model of multiple sclerosis with upregulation of PPAR-γ expression.
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Behairy Shereen F, Fahmy Mohamed I, Sayed Rabab H, El-Yamany Mohammed F
Аннотация
OBJECTIVES: To investigate the effects of naringenin on pathological, molecular, and behavioural alterations in a cuprizone-induced mouse model of demyelination, with particular emphasis on peroxisome proliferator-activated receptor (PPAR) gamma expression, NOD-like receptor family pyrin domain-containing 3 immunoreactivity, and molecular markers of myelin integrity, inflammation, and apoptosis.
METHODS: Mice were allocated to four groups: control, naringenin alone, cuprizone, and cuprizone plus naringenin. Demyelination was induced with cuprizone-containing chow, and naringenin was administered orally for three weeks. Motor performance and biochemical, molecular, and histological changes were evaluated using established behavioural, immunological, molecular, and histological techniques.
KEY FINDINGS: Naringenin improved motor deficits, increased myelin basic protein expression, reduced tumour necrosis factor-alpha, interleukin-1 beta, cyclooxygenase-2, prostaglandin E2, and nuclear factor kappa B p65 levels, and shifted apoptotic signalling towards cell survival by decreasing Bcl-2-associated X and increasing B-cell lymphoma 2 expression. Naringenin also increased PPAR gamma expression while reducing NOD-like receptor family pyrin domain-containing 3 immunoreactivity and suppressor of cytokine signalling 3 expression.
CONCLUSIONS: Naringenin attenuated cuprizone-induced brain inflammatory responses, apoptosis, and myelin injury, with findings consistent with modulation of PPAR gamma expression and NOD-like receptor family pyrin domain-containing 3-associated neuroinflammatory responses. These findings support further preclinical evaluation of naringenin for multiple sclerosis.
METHODS: Mice were allocated to four groups: control, naringenin alone, cuprizone, and cuprizone plus naringenin. Demyelination was induced with cuprizone-containing chow, and naringenin was administered orally for three weeks. Motor performance and biochemical, molecular, and histological changes were evaluated using established behavioural, immunological, molecular, and histological techniques.
KEY FINDINGS: Naringenin improved motor deficits, increased myelin basic protein expression, reduced tumour necrosis factor-alpha, interleukin-1 beta, cyclooxygenase-2, prostaglandin E2, and nuclear factor kappa B p65 levels, and shifted apoptotic signalling towards cell survival by decreasing Bcl-2-associated X and increasing B-cell lymphoma 2 expression. Naringenin also increased PPAR gamma expression while reducing NOD-like receptor family pyrin domain-containing 3 immunoreactivity and suppressor of cytokine signalling 3 expression.
CONCLUSIONS: Naringenin attenuated cuprizone-induced brain inflammatory responses, apoptosis, and myelin injury, with findings consistent with modulation of PPAR gamma expression and NOD-like receptor family pyrin domain-containing 3-associated neuroinflammatory responses. These findings support further preclinical evaluation of naringenin for multiple sclerosis.