Neuroprotective effect of preadministration with Ganoderma lucidum spore on rat hippocampus

• Published in: Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie Vol. 64; no. 7-8; pp. 673 - 680
• Main Authors: Zhou, Yan, Qu, Ze-qiang, Zeng, Yuan-shan, Lin, Yu-kun, Li, Yan, Chung, Peter, Wong, Ricky, Hägg, Urban
• Format: Journal Article
• Language: English
• Published: Munich Elsevier GmbH 01-11-2012; Elsevier
• Subjects: adenosine triphosphate; Adult and adolescent clinical studies; Alzheimer disease; Alzheimer's disease; Animals; apoptosis; Apoptosis - drug effects; Behavior, Animal - drug effects; Biological and medical sciences; Brain Mapping; cognition; cytochrome-c oxidase; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Dose-Response Relationship, Drug; Drug Administration Schedule; energy metabolism; Energy Metabolism - drug effects; Ganoderma lucidum; glutathione; glutathione-disulfide reductase; hippocampus; Hippocampus - drug effects; Hippocampus - enzymology; Hippocampus - metabolism; Hippocampus - pathology; histopathology; Injections, Intraventricular; Intracerebroventricular streptozotocin; Investigative techniques, diagnostic techniques (general aspects); Learning and memory; Male; malondialdehyde; Maze Learning - drug effects; Medical sciences; memory; Microscopy, Electron; Microscopy, Fluorescence; Mitochondria - drug effects; Mitochondria - metabolism; Neurology; neurons; Neurons - drug effects; Neurons - metabolism; Neurons - pathology; Neuroprotective Agents - administration & dosage; Neuroprotective Agents - isolation & purification; Neuroprotective Agents - pharmacology; Neuroprotective effect; Organic mental disorders. Neuropsychology; Oxidative stress; Oxidative Stress - drug effects; pathogenesis; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Rats; Rats, Sprague-Dawley; Reishi - chemistry; Reishi - physiology; spores; Spores, Fungal - chemistry; Streptozocin - toxicity; streptozotocin; Learning and memory; Intracerebroventricular streptozotocin; Oxidative stress; Neuroprotective effect; Ganoderma lucidum; Alzheimer's disease; Animal model; Neuroprotection; Rat; Alzheimer disease; Memory; Central nervous system; Spores; Basidiomycota; Encephalon; Fungi; Learning; Acquisition process; Degenerative disease; Streptozotocin; Ganoderma; Nervous system diseases; Rodentia; Cerebral disorder; Vertebrata; Anatomic pathology; Mammalia; Animal; Central nervous system disease; Hippocampus
• ISSN: 0940-2993; 1618-1433
• DOI: 10.1016/j.etp.2010.12.011

The aim of this study was to investigate if preadministration with Ganoderma lucidum spore (GLS) could (1) alleviate oxidative stress and mitochondrial dysfunction in rat hippocampus of intracerebroventricular (ICV) injection of streptozotocin (STZ), (2) protect neurons from apoptosis, and (3) improve cognitive dysfunction. Three groups of Sprague–Dawley rats were preadministrated with GLS at doses of 2.0, 4.0 and 8.0g/kg, respectively, for 3 weeks before the ICV STZ injury. Thereafter the rats were operated with ICV STZ (1.5mg/kg) bilaterally on days 1 and 3. The behavioral alterations, oxidative stress indexes, ATP, cytochrome oxidase (CytOx), and histopathology of hippocampal neurons were studied. The results showed that ICV STZ model rats exhibited a significant increase of malondialdehyde (MDA), a significant decrease of glutathione reductase (GR), reduced glutathione (GSH), ATP and CytOx, accompanied with marked impairments in spatial learning and memory, and severe damage of hippocampal neuron. In conclusion, preadministration with GLS at dose of 8.0g/kg in ICV STZ rats significantly reversed these abnormalities. In conclusion, preadministration with GLS might protect hippocampus from oxidative impairment and energy metabolism disturbance of ICV STZ. This may also provide useful information for future research on the pathogenesis and prevention of Alzheimer's disease (AD).