Tissue & cell · 2026
Matcha green tea attenuates acrylamide-induced cerebellar damage in rats: Biochemical, histological and immunohistochemical study.
СтатьяНазвание и аннотация: Перевод в очереди
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.
Essawy Asmaa S, Abo Elkhair Doaa M
Аннотация
In industry, acrylamide (ACR) is generated by heating tobacco and carbohydrate-rich foods. In the past decade, ACR neurotoxicity has become a growing concern. This study examined matcha green tea (MAT)'s protective effect against cerebellar toxicity induced by ACR and its neuroprotective mechanisms in rats. Forty male albino rats were divided randomly into four experimental groups: control group, MAT group (150 mg/kg), ACR group (50 mg/kg), and ACR + MAT group. Oxidative stress and inflammatory biomarkers in cerebellar tissue (superoxide dismutase; SOD, catalase; CAT, glutathione peroxidase; GPx, malondialdehyde; MDA, tumor necrosis factor-alpha; TNF-α and Interleukin 6; IL-6) were assessed. Cerebellar tissues were exposed to histological, immunohistochemical, and ultrastructural evaluations. Significant decline in the SOD, CAT, and GPx levels together with significant rise in the levels of MDA, TNF-α, and IL-6 were observed in ACR group. Histologically, the ACR group showed variable degrees of cellular degeneration with marked reduction of Nissl's granules. This was verified by electron microscopic examination and strong positive reaction for GFAP, NF-κB and caspase -3. Rats treated by ACR + MAT showed improvement of the biochemical, histological and ultrastructural parameters. This was confirmed by the significant diminution in caspase-3, NF-κB & GFAP immunostaining. In conclusion, matcha green tea amended the alterations in the cerebellum induced by ACR through modulation of inflammation, oxidative stress and apoptosis.