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<p>Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, oxidative stress, neuroinflammation, and neuronal loss. This study evaluated the neuroprotective potential of berberine chloride (BC) against D-Galactose (D-Gal) and aluminum chloride (AlCl<sub>3</sub>)-induced Alzheimer-like neurodegeneration models in rats using donepezil as a standard drug. Animals were randomly assigned into four groups: control, AD-model (D-Gal 60&#xa0;mg/kg/day, i.p.+AlCl<sub>3</sub> 200&#xa0;mg/kg/day, orally), BC-treated (100&#xa0;mg/kg/day), and donepezil-treated (2&#xa0;mg/kg/day). The AD model exhibited significant cognitive deficits, evidenced by reduced spontaneous alternation (39%↓), prolonged escape latency (38%↑), and diminished locomotor activity. BC markedly enhanced endogenous antioxidant defense, elevating superoxide dismutase and catalase activities by 165% and 145% (<i>p</i> &lt; 0.05), while reducing lipid peroxidation and nitric oxide levels in brain tissue (67%↓). BC also markedly suppressed advanced glycation end (AGEs) products by 37% (<i>p</i> &lt; 0.05). Furthermore, BC improved cholinergic function by significantly lowering serum acetylcholinesterase activity (30%↓) and ameilorated hepatic and renal biochemical indices-AST (42%↓), ALT (55%↓), and urea (55%↓). Histopathological examination revealed preservation of hippocampal and cortical neuronal architecture, with reduced neurodegeneration and gliosis in BC-treated animals. Collectively, these findings demonstrate that BC exerts potent neuroprotective, antioxidant, anti-glycation, and anti-inflammatory effects, highlighting its promise as a multi-target candidate for cognitive impairment.</p>

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Neuromodulatory effects of berberine chloride against aluminum chloride/D-Galactose induced Alzheimer-like neurodegeneration model in rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月14日

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  • Adedoyin O. Adefisan-Adeoye,
  • Heritage Oluwadamilare,
  • Mary Aisedion,
  • Toyin S. Shittu,
  • Tare Amangele,
  • Temitope D. Adeoye,
  • Jeremiah O. Unuofin,
  • Bukunmi M. Orimolade,
  • Sogolo L. Lebelo,
  • Oluwatosin A. Adaramoye

摘要

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, oxidative stress, neuroinflammation, and neuronal loss. This study evaluated the neuroprotective potential of berberine chloride (BC) against D-Galactose (D-Gal) and aluminum chloride (AlCl3)-induced Alzheimer-like neurodegeneration models in rats using donepezil as a standard drug. Animals were randomly assigned into four groups: control, AD-model (D-Gal 60 mg/kg/day, i.p.+AlCl3 200 mg/kg/day, orally), BC-treated (100 mg/kg/day), and donepezil-treated (2 mg/kg/day). The AD model exhibited significant cognitive deficits, evidenced by reduced spontaneous alternation (39%↓), prolonged escape latency (38%↑), and diminished locomotor activity. BC markedly enhanced endogenous antioxidant defense, elevating superoxide dismutase and catalase activities by 165% and 145% (p < 0.05), while reducing lipid peroxidation and nitric oxide levels in brain tissue (67%↓). BC also markedly suppressed advanced glycation end (AGEs) products by 37% (p < 0.05). Furthermore, BC improved cholinergic function by significantly lowering serum acetylcholinesterase activity (30%↓) and ameilorated hepatic and renal biochemical indices-AST (42%↓), ALT (55%↓), and urea (55%↓). Histopathological examination revealed preservation of hippocampal and cortical neuronal architecture, with reduced neurodegeneration and gliosis in BC-treated animals. Collectively, these findings demonstrate that BC exerts potent neuroprotective, antioxidant, anti-glycation, and anti-inflammatory effects, highlighting its promise as a multi-target candidate for cognitive impairment.