Neuroprotective effects of astaxanthin in a scopolamine-induced rat model of Alzheimer’s disease through antioxidant/anti-inflammatory pathways and opioid/benzodiazepine receptors: attenuation of Nrf2, NF-κB, and interconnected pathways DOI Creative Commons

Zeinab Rastinpour,

Sajad Fakhri, Fatemeh Abbaszadeh

и другие.

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Май 15, 2025

Given the complexity of pathological mechanisms behind Alzheimer's disease (AD), there is a pressing need for novel multi-targeting therapeutic agents. Astaxanthin, natural compound with diverse biological effects, has emerged as potential candidate in neuronal diseases. This study aimed to evaluate neuroprotective effects astaxanthin scopolamine-induced rat model AD. In total, 36 male Wistar rats were divided into six groups, including control group receiving normal saline, negative treated scopolamine (1 mg/kg), and two groups at doses 5 10 mg/kg. Additionally, pre-treated naloxone (0.1 mg/kg) or flumazenil (0.5 block opioid benzodiazepine receptors, respectively, followed by most effective dose (i.e., mg/kg). Treatments administered via intraperitoneal injection 14 consecutive days behavioral tests done. Biochemical analyses, zymography, Western blotting, histopathological examinations also performed. Astaxanthin treatment significantly improved cognitive function, enhanced plasma antioxidant capacity increasing catalase glutathione levels, reduced nitrite levels. It increased serum activity matrix metalloproteinase 2 (MMP-2), while decreasing MMP-9, expression nuclear factor erythroid 2-related (Nrf-2) kappa B (NF-κB) hippocampal tissue. Histopathological findings indicated damage after administration. The aforementioned protective reversed flumazenil. demonstrates against AD through its neuroprotective, antioxidant, anti-inflammatory properties, potentially involving interactions receptors.

Язык: Английский

Neuroprotective effects of astaxanthin in a scopolamine-induced rat model of Alzheimer’s disease through antioxidant/anti-inflammatory pathways and opioid/benzodiazepine receptors: attenuation of Nrf2, NF-κB, and interconnected pathways DOI Creative Commons

Zeinab Rastinpour,

Sajad Fakhri, Fatemeh Abbaszadeh

и другие.

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Май 15, 2025

Given the complexity of pathological mechanisms behind Alzheimer's disease (AD), there is a pressing need for novel multi-targeting therapeutic agents. Astaxanthin, natural compound with diverse biological effects, has emerged as potential candidate in neuronal diseases. This study aimed to evaluate neuroprotective effects astaxanthin scopolamine-induced rat model AD. In total, 36 male Wistar rats were divided into six groups, including control group receiving normal saline, negative treated scopolamine (1 mg/kg), and two groups at doses 5 10 mg/kg. Additionally, pre-treated naloxone (0.1 mg/kg) or flumazenil (0.5 block opioid benzodiazepine receptors, respectively, followed by most effective dose (i.e., mg/kg). Treatments administered via intraperitoneal injection 14 consecutive days behavioral tests done. Biochemical analyses, zymography, Western blotting, histopathological examinations also performed. Astaxanthin treatment significantly improved cognitive function, enhanced plasma antioxidant capacity increasing catalase glutathione levels, reduced nitrite levels. It increased serum activity matrix metalloproteinase 2 (MMP-2), while decreasing MMP-9, expression nuclear factor erythroid 2-related (Nrf-2) kappa B (NF-κB) hippocampal tissue. Histopathological findings indicated damage after administration. The aforementioned protective reversed flumazenil. demonstrates against AD through its neuroprotective, antioxidant, anti-inflammatory properties, potentially involving interactions receptors.

Язык: Английский

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