Genistein Suppresses the Mitochondrial Apoptotic Pathway in Hippocampal Neurons in Rats with Alzheimer's Disease
Open accessAbstract
Genistein is effective against amyloid-β toxicity, but the underlying mechanisms are unclear. We hypothesized that genistein may protect neurons by inhibiting the mitochondrial apoptotic pathway, and thereby play a role in the prevention of Alzheimer's disease. A rat model of Alzheimer's disease was established by intraperitoneal injection of D-galactose and intracerebral injection of amyloid-β peptide (25-35). In the genistein treatment groups, a 7-day pretreatment with genistein (10, 30, 90 mg/kg) was given prior to establishing Alzheimer's disease model, for 49 consecutive days. Terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labeling assay demonstrated a reduction in apoptosis in the hippocampus of rats treated with genistein. Western blot analysis showed that expression levels of capase-3, Bax and cytochrome c were decreased compared with the model group. Furthermore, immunohistochemical staining revealed reductions in cytochrome c and Bax immunoreactivity in these rats. Morris water maze revealed a substantial shortening of escape latency by genistein in Alzheimer's disease rats. These findings suggest that genistein decreases neuronal loss in the hippocampus, and improves learning and memory ability. The neuroprotective effects of genistein are associated with the inhibition of the mitochondrial apoptotic pathway, as shown by its ability to reduce levels of caspase-3, Bax and cytochrome c.
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In diabetic mice, genistein and some derivatives improve cognitive dysfunction by inhibiting AChE and modulating Ca2+ homeostasis in cholinergic neurons.
“in diabetic mice genistein (Pedersen et al., 1996; Wang et al., 2016), as well as some of its derivatives (Qiang et al., 2014), can improve cognitive dysfunction by inhibiting the activity of AChE and by the modulation of Ca2+ homeostasis in cholinergic neurons (Jhamandas et al., 2001)”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Wang et al., 2016
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- Authors
- Cai, B., Wang, Y., Shao, J., Wang, T.-T., Cai, R.-Z., Ma, C.-J., Han, T., & Du, J.
- Affiliations
- Anhui University of Traditional Chinese Medicine (CN)
- Corresponding author
- Cai, Biao
- Venue
- Neural Regeneration Research
- Published
- 2016
- Volume
- 11
- Issue
- 7
- Pages
- 1153
- ISSN
- 1673-5374 (ISSN-L)
- PMC
- PMC4994461
- OpenAlex
- W2497199157
- Cited by
- 52
- References
- 35
- Citations by year
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- FWCI
- 5.10
- Type
- journal article
- Language
- en
- Update notices
- correction (2024-11-01)
- Open access
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- doi.org
- Licence
- cc-by-nc-sa
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- Neural Regeneration Research (publishedVersion, cc-by-nc-sa)
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- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Keywords
- genistein, Alzheimer's disease, mitochondrial apoptosis, hippocampal neurons, neuroprotection, amyloid-beta, galactose, caspase-3, Bax, cytochrome c, learning and memory, neuronal loss
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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