Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
Niosomal hesperidin ameliorates depression-induced behavioral, histological, and molecular alterations in the rat hippocampus.
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.
Otarkhani Mahsa, Hatami Homeira, Panahi Yousef, Jammal Abdallah Al, Sadeghian Reihaneh, Yavari Sama
Аннотация
AIM: Niosomal carriers offer a promising drug delivery in neurological disorders. This study evaluated the therapeutic effects of niosome-encapsulated hesperidin on reserpine-induced depression in rats, focusing on oxidative stress, transient receptor potential melastatin2 (TRPM2) and transient receptor potential canonical 1(TRPC1) gene expression levels, and histo-striology changes in hippocampal tissue.
METHODS: 36 rats were randomly divided into six groups, including Control, Depression, Hes (Hesperidin), nHes (Niosomes of Hesperidin), Dep+Hes, and Dep+nHes. Reserpine 0.5 mg/kg was administered intraperitoneally to induce the Dep Model for 14 days. Then, with intraperitoneal injection, rats received Hes (20 mg/kg for 14 days) and nHes (20 mg/kg for 7 days). Next, the Forced Swimming Test (FST) and the Sucrose Preference Test (SPT) were applied to assess Behavioral disorders. Finally, Glutathione peroxidase (GPX) levels, malondialdehyde (MDA), TRPM2, and TRPC1 gene expression, as well as histo-stereological studies, were measured in hippocampal tissue.
RESULTS: The nHSP treatment reduced immobility duration and increased sucrose solution consumption compared to the depression group in behavioral tests. The expression of genes TRPM2 decreased in the Dep+nHSP group compared with the depression group, and TRPC1 decreased in the HSP group compared with the depression group. Histological and stereological studies revealed improved apoptosis and cell death in nHSP-treated rats, with an increase in live cells compared to the depressed group.
CONCLUSION: Our findings suggest that nHes improves depression phenotypes induced by reserpine by reducing hippocampal oxidative stress damage and histopathological alterations. This may be related to enhanced therapeutic efficacy and bioavailability due to liposomal carriers.
METHODS: 36 rats were randomly divided into six groups, including Control, Depression, Hes (Hesperidin), nHes (Niosomes of Hesperidin), Dep+Hes, and Dep+nHes. Reserpine 0.5 mg/kg was administered intraperitoneally to induce the Dep Model for 14 days. Then, with intraperitoneal injection, rats received Hes (20 mg/kg for 14 days) and nHes (20 mg/kg for 7 days). Next, the Forced Swimming Test (FST) and the Sucrose Preference Test (SPT) were applied to assess Behavioral disorders. Finally, Glutathione peroxidase (GPX) levels, malondialdehyde (MDA), TRPM2, and TRPC1 gene expression, as well as histo-stereological studies, were measured in hippocampal tissue.
RESULTS: The nHSP treatment reduced immobility duration and increased sucrose solution consumption compared to the depression group in behavioral tests. The expression of genes TRPM2 decreased in the Dep+nHSP group compared with the depression group, and TRPC1 decreased in the HSP group compared with the depression group. Histological and stereological studies revealed improved apoptosis and cell death in nHSP-treated rats, with an increase in live cells compared to the depressed group.
CONCLUSION: Our findings suggest that nHes improves depression phenotypes induced by reserpine by reducing hippocampal oxidative stress damage and histopathological alterations. This may be related to enhanced therapeutic efficacy and bioavailability due to liposomal carriers.