Neurological research · 2025
Alpha-asarone protects against rotenone-induced neurotoxicity in a rat model of Parkinson's disease.
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.
Kaur Satinder, Hussain Md Sadique, Bahl Gurusha, Kumar Rajesh, Khurana Navneet, Kumar Rajan, Kakoty Violina, Pal Biplab, Ali Nemat, AlAsmari Abdullah F, Al-Rejaie Salim S, Waseem Mohammad, Sharma Neha
Аннотация
OBJECTIVES: This study aimed to evaluate the neuroprotective effects of alpha-asarone on biochemical, behavioral, neurochemical, and histopathological alterations induced by rotenone in a rat model of Parkinson's disease (PD).
METHODS: Male rats were divided into six groups: control, alpha-asarone alone (15 mg/kg, oral), rotenone alone (2 mg/kg, subcutaneous), rotenone with levodopa + carbidopa (15 + 3.75 mg/kg, oral), and rotenone with alpha-asarone at two doses (7.5 and 15 mg/kg, oral). Treatments were administered for 35 days. Behavioral assessments included catalepsy, rearing behavior, postural instability, locomotor activity, muscle coordination, grip strength, beam walk latency, and general movement analysis. Biochemical assays measured levels of TBARS, SAG, GSH, and CAT. Dopamine levels were assessed neurochemically, and histopathological analysis was conducted on brain tissue.
RESULTS: Alpha-asarone significantly reversed rotenone-induced behavioral impairments and improved performance across various motor and coordination tests. Biochemically, alpha-asarone reduced TBARS and SAG levels while increasing GSH and CAT, indicating enhanced antioxidant defense. It also restored dopamine levels reduced by rotenone. Histopathological analysis showed fewer eosinophilic lesions in alpha-asarone co-treated rats compared to the rotenone-only group.
DISCUSSION: The results suggest that alpha-asarone exerts protective effects against rotenone-induced neurotoxicity in PD through antioxidant and dopaminergic mechanisms. By improving behavioral outcomes, reducing oxidative stress, and preserving neuronal integrity, alpha-asarone demonstrates potential as an anti-Parkinsonian agent. Further studies are needed to confirm its therapeutic applicability and elucidate its precise molecular targets.
METHODS: Male rats were divided into six groups: control, alpha-asarone alone (15 mg/kg, oral), rotenone alone (2 mg/kg, subcutaneous), rotenone with levodopa + carbidopa (15 + 3.75 mg/kg, oral), and rotenone with alpha-asarone at two doses (7.5 and 15 mg/kg, oral). Treatments were administered for 35 days. Behavioral assessments included catalepsy, rearing behavior, postural instability, locomotor activity, muscle coordination, grip strength, beam walk latency, and general movement analysis. Biochemical assays measured levels of TBARS, SAG, GSH, and CAT. Dopamine levels were assessed neurochemically, and histopathological analysis was conducted on brain tissue.
RESULTS: Alpha-asarone significantly reversed rotenone-induced behavioral impairments and improved performance across various motor and coordination tests. Biochemically, alpha-asarone reduced TBARS and SAG levels while increasing GSH and CAT, indicating enhanced antioxidant defense. It also restored dopamine levels reduced by rotenone. Histopathological analysis showed fewer eosinophilic lesions in alpha-asarone co-treated rats compared to the rotenone-only group.
DISCUSSION: The results suggest that alpha-asarone exerts protective effects against rotenone-induced neurotoxicity in PD through antioxidant and dopaminergic mechanisms. By improving behavioral outcomes, reducing oxidative stress, and preserving neuronal integrity, alpha-asarone demonstrates potential as an anti-Parkinsonian agent. Further studies are needed to confirm its therapeutic applicability and elucidate its precise molecular targets.