Dose-response : a publication of International Hormesis Society · 2026
Cnicin Attenuates Aluminium Chloride-Induced Neurodegeneration Through Antioxidant and Anti-Inflammatory Mechanisms.
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Yu Li, Alhoqail Wardah A, Mickymaray Suresh, Li Fang
Аннотация
BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disorder with limited disease-modifying therapies. Aluminium chloride (AlCl3)-induced neurotoxicity mimics key pathological features of AD, including oxidative stress, neuroinflammation, and cholinergic dysfunction.
OBJECTIVE: This study aimed to evaluate the neuroprotective effect of cnicin in an AlCl3-induced rat model of Alzheimer-like neurodegeneration.
METHODS: Rats were divided into five groups: normal control, AlCl3 control (75 mg/kg/day, p.o.), AlCl3 with cnicin (20 and 40 mg/kg/day, p.o.), and AlCl3 with donepezil (5 mg/kg/day, p.o.) for 30 days. Behavioral performance was assessed using hanging wire and beam walking tests. Biochemical parameters, including acetylcholinesterase (AChE), antioxidant enzymes (SOD, CAT, GSH), malondialdehyde (MDA), and inflammatory cytokines (TNF-α, IL-1β) were analyzed, along with histopathology.
RESULTS: AlCl3 administration induced significant behavioral deficits, increased AChE activity, oxidative stress, neuroinflammation, and neuronal damage. Cnicin treatment dose-dependently improved motor function, reduced AChE activity, restored antioxidant levels, decreased lipid peroxidation, and suppressed inflammatory markers. Histological analysis confirmed preservation of neuronal architecture, comparable to that of donepezil.
CONCLUSION: Cnicin exhibits significant neuroprotective effects against AlCl3-induced neurodegeneration by modulating cholinergic activity, oxidative stress, and inflammation, suggesting its potential as a therapeutic agent for AD.
OBJECTIVE: This study aimed to evaluate the neuroprotective effect of cnicin in an AlCl3-induced rat model of Alzheimer-like neurodegeneration.
METHODS: Rats were divided into five groups: normal control, AlCl3 control (75 mg/kg/day, p.o.), AlCl3 with cnicin (20 and 40 mg/kg/day, p.o.), and AlCl3 with donepezil (5 mg/kg/day, p.o.) for 30 days. Behavioral performance was assessed using hanging wire and beam walking tests. Biochemical parameters, including acetylcholinesterase (AChE), antioxidant enzymes (SOD, CAT, GSH), malondialdehyde (MDA), and inflammatory cytokines (TNF-α, IL-1β) were analyzed, along with histopathology.
RESULTS: AlCl3 administration induced significant behavioral deficits, increased AChE activity, oxidative stress, neuroinflammation, and neuronal damage. Cnicin treatment dose-dependently improved motor function, reduced AChE activity, restored antioxidant levels, decreased lipid peroxidation, and suppressed inflammatory markers. Histological analysis confirmed preservation of neuronal architecture, comparable to that of donepezil.
CONCLUSION: Cnicin exhibits significant neuroprotective effects against AlCl3-induced neurodegeneration by modulating cholinergic activity, oxidative stress, and inflammation, suggesting its potential as a therapeutic agent for AD.