Iranian journal of basic medical sciences · 2026
Rutin attenuates cuprizone-induced demyelination in C57BL/6 mice through activation of Nrf2 signaling and inhibition of NF-κB.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Alavi Seyede Darya, Shirooie Samira, Sureda Antoni, Farzaei Mohammad Hosein, Fakhri Sajad, Asgary Sedigheh
Аннотация
OBJECTIVES: Multiple sclerosis (MS) is a debilitating demyelinating disease characterized by oxidative stress and neuroinflammation. This study investigated the therapeutic potential of rutin, a natural flavonoid, in a cuprizone (CPZ)-induced mouse model of demyelination.
MATERIALS AND METHODS: Male C57BL/6 mice were fed a 0.2% CPZ diet for six weeks to induce central nervous system demyelination and were concurrently treated with rutin (50 or 100 mg/kg, intraperitoneally, for the last 14 days). Behavioral assessments, histochemical examinations, and immunohistochemistry for Nrf2, HO-1, NQO-1, and NF-kB p65 were then performed.
RESULTS: Behavioral tests revealed that rutin dose-dependently improved CPZ-induced motor coordination deficits in the pole, rotarod, and open-field tests. Histological analysis (LFB and H&E staining) demonstrated that rutin significantly attenuated demyelination in the corpus callosum. Mechanistically, immunohistochemistry showed that rutin treatment effectively up-regulated the key antioxidant pathway by increasing the expression of phosphorylated Nrf2 (p-Nrf2) and its downstream targets (HO-1 and NQO-1), while simultaneously suppressing the pro-inflammatory NF-κB p65 pathway.
CONCLUSION: Our findings show that rutin protects against demyelination through a dual mechanism of enhancing endogenous anti-oxidant defenses and inhibiting neuroinflammation, highlighting it as a promising candidate for further studies on demyelinating disorders such as MS.
MATERIALS AND METHODS: Male C57BL/6 mice were fed a 0.2% CPZ diet for six weeks to induce central nervous system demyelination and were concurrently treated with rutin (50 or 100 mg/kg, intraperitoneally, for the last 14 days). Behavioral assessments, histochemical examinations, and immunohistochemistry for Nrf2, HO-1, NQO-1, and NF-kB p65 were then performed.
RESULTS: Behavioral tests revealed that rutin dose-dependently improved CPZ-induced motor coordination deficits in the pole, rotarod, and open-field tests. Histological analysis (LFB and H&E staining) demonstrated that rutin significantly attenuated demyelination in the corpus callosum. Mechanistically, immunohistochemistry showed that rutin treatment effectively up-regulated the key antioxidant pathway by increasing the expression of phosphorylated Nrf2 (p-Nrf2) and its downstream targets (HO-1 and NQO-1), while simultaneously suppressing the pro-inflammatory NF-κB p65 pathway.
CONCLUSION: Our findings show that rutin protects against demyelination through a dual mechanism of enhancing endogenous anti-oxidant defenses and inhibiting neuroinflammation, highlighting it as a promising candidate for further studies on demyelinating disorders such as MS.