Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
Aprepitant's neuroprotective effects on methylphenidate-induced biochemical/mitochondrial dysfunction, neuroinflammation, and mood-related behavior alterations.
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.
Akbarpournikghalb Ladan, Pourdehghan Shahrestani Parisa, Gomi Mahnaz, Hayes A Wallace, Gholami Mahdieh, Motaghinejad Majid
Аннотация
BACKGROUND: Chronic methylphenidate (MPH) use causes neurological and behavioral problems. Aprepitant (APR) has demonstrated neuroprotective effects.
OBJECTIVES: This research investigated APR's neuroprotective effects against MPH-induced biochemical, mitochondrial, motor, and mood disturbances in rats.
METHOD: Forty-eight male Wistar rats were divided into six groups to receive treatment for 21 days with saline, MPH, or different doses of APR combined with MPH. Behavioral tests included OFT, EPM, and FST; biochemical assessments focused on hippocampal inflammation, oxidative stress, and apoptosis pathways.
RESULTS: APR dose-dependently mitigated the MPH-induced disruptions in motor activity and mood, and increased activities of glutathione peroxidase (GPx), glutathione reductase (GR), and superoxide dismutase (SOD), along with levels of mitochondrial membrane potential (ΔΨm = MMP), reduced glutathione (GSH), total antioxidant capacity (TAC), adenosine triphosphate (ATP), and unphosphorylated Bcl-2. In MPH-treated rats, APR decreased tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β), oxidized glutathione (GSSG), reactive oxygen species (ROS), malondialdehyde (MDA), and hydrogen peroxide (H2O2), and reduced both forms of JNK, Bax, Beclin-1, and phosphorylated Bcl-2.
CONCLUSION: APR dose-dependently alleviated MPH-induced anxiety and depression-like behaviors, restored redox and mitochondrial homeostasis, suppressed MPH-induced neuroinflammation and neuronal apoptosis, and influenced Beclin, a key regulator of autophagosome nucleation.
OBJECTIVES: This research investigated APR's neuroprotective effects against MPH-induced biochemical, mitochondrial, motor, and mood disturbances in rats.
METHOD: Forty-eight male Wistar rats were divided into six groups to receive treatment for 21 days with saline, MPH, or different doses of APR combined with MPH. Behavioral tests included OFT, EPM, and FST; biochemical assessments focused on hippocampal inflammation, oxidative stress, and apoptosis pathways.
RESULTS: APR dose-dependently mitigated the MPH-induced disruptions in motor activity and mood, and increased activities of glutathione peroxidase (GPx), glutathione reductase (GR), and superoxide dismutase (SOD), along with levels of mitochondrial membrane potential (ΔΨm = MMP), reduced glutathione (GSH), total antioxidant capacity (TAC), adenosine triphosphate (ATP), and unphosphorylated Bcl-2. In MPH-treated rats, APR decreased tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β), oxidized glutathione (GSSG), reactive oxygen species (ROS), malondialdehyde (MDA), and hydrogen peroxide (H2O2), and reduced both forms of JNK, Bax, Beclin-1, and phosphorylated Bcl-2.
CONCLUSION: APR dose-dependently alleviated MPH-induced anxiety and depression-like behaviors, restored redox and mitochondrial homeostasis, suppressed MPH-induced neuroinflammation and neuronal apoptosis, and influenced Beclin, a key regulator of autophagosome nucleation.