What question did this study set out to answer?

To determine if berberine can reduce cognitive and emotional impairments caused by single prolonged stress.

June 11, 2026Nutritional Neuroscience0 citations

Berberine attenuates SPS-induced cognitive and affective deficits and corticolimbic injury in Wistar rats via restoration of BDNF and redox–inflammatory balance

GAGodson Emeka AnyanwuKampala International University PEPrecious E. EkwuemeUniversity of Nigeria ANAyugha NsanUniversity of Nigeria

Key Points

To determine if berberine can reduce cognitive and emotional impairments caused by single prolonged stress.
Adult male Wistar rats exposed to single prolonged stress and left undisturbed for 7 days.
Rats administered oral berberine (50 or 200 mg/kg) or fluoxetine (10 mg/kg) daily.
Behavior measured using Y-maze, Morris water maze, novel object recognition, and ELISA for serum corticosterone.
SPS caused significant memory and reward sensitivity deficits with elevated corticosterone.
Berberine improved behavioral outcomes and normalized corticosterone levels, BDNF, and reduced pro-inflammatory markers.
Histopathological analysis showed reduced neuroinflammation and enhanced neuronal integrity with berberine treatment.

Abstract

BACKGROUND: Single prolonged stress (SPS) is a validated PTSD-like paradigm that causes cognitive and affective dysfunction and corticolimbic injuries due to the dysregulation of the HPA-axis and neurotrophic, redox, and neuroimmune pathways. Berberine is a bioactive isoquinoline alkaloid that demonstrates neuroprotective effects, although its effect on corticolimbic-pathology caused by SPS is yet to be fully characterized. OBJECTIVES: To ascertain whether berberine attenuates SPS-induced neurobehavioral impairments and corticolimbic neuronal damage in Wistar rats. METHODS: Adult male Wistar rats were exposed to SPS (restraint, forced swim, and anesthetic-induced loss of consciousness) and left undisturbed for 7 days to allow stress consolidation. Then, rats were given oral berberine (50 or 200 mg/kg) or fluoxetine (10 mg/kg) in a single daily dose. Behavioral measures were Y-maze spontaneous alternation, Morris water maze, novel object recognition and sucrose preference. ELISA was used to quantify serum corticosterone. BDNF, SOD, catalase, MDA, and IL-1b/IL-6/TNF-a were assayed in the hippocampus and mPFC. CFV and NeuN immunohistochemistry were used to assess neuronal integrity and astrocytic reactivity was assessed using GFAP-immunoreactivity. RESULTS: SPS induced severe deficits in working memory, spatial and recognition memories and reward sensitivity, and high basal corticosterone. It increased lipid peroxidation and pro-inflammatory cytokines while reducing antioxidant enzyme activities in brain tissue homogenates (hippocampus and medial prefrontal cortex). Berberine improved behavioral outcomes and attenuated endocrine, biochemical, and histopathological abnormalities in a dose-dependent manner. CONCLUSION: Berberine attenuates SPS-induced-cognitive/affective dysfunction and corticolimbic-lesion and establishes normalization of basal corticosterone, BDNF recovery, antioxidant defense, lipid peroxidation, cytokine elevations, and astrocytic activation. These findings support berberine as a multi-target candidate for mitigating stress-related-neurotoxicity.

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