ArticleNeurochemical research2011
Extract from Terminalia chebula seeds protect against experimental ischemic neuronal damage via maintaining SODs and BDNF levels.
Article in Neurochemical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 63 citations in OpenAlex.
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- Impact of dietary polyphenols on neuroinflammation-associated disorders.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Review
- Use of medicinal plants for headache, and their potential implication in medication-overuse headache: Evidence from a population-based study in Nepal.Cephalalgia : an international journal of headache · 2021Article
- Traditional Herbal Medicines Against CNS Disorders from Bangladesh.Natural products and bioprospecting · 2020Review
- Putative Roles of Plant-Derived Tannins in Neurodegenerative and Neuropsychiatry Disorders: An Updated Review.Molecules (Basel, Switzerland) · 2019Review
- Ginsenoside Rb2 suppresses the glutamate-mediated oxidative stress and neuronal cell death in HT22 cells.Journal of ginseng research · 2019Article
- Corilagin induces the apoptosis of hepatocellular carcinoma cells through the mitochondrial apoptotic and death receptor pathways.Oncology reports · 2018Article
- Age‑dependent decreases in insulin‑like growth factor‑I and its receptor expressions in the gerbil olfactory bulb.Molecular medicine reports · 2018Article
- Antioxidant and pro-angiogenic effects of corilagin in rat cerebral ischemia via Nrf2 activation.Oncotarget · 2017Article
- PretreatedChinese medical journal · 2017Article
- Pretreated quercetin protects gerbil hippocampal CA1 pyramidal neurons from transient cerebral ischemic injury by increasing the expression of antioxidant enzymes.Neural regeneration research · 2017Article
- NEUROPROTECTIVE EFFECT OFAfrican journal of traditional, complementary, and alternative medicines : AJTCAM · 2017Article
- New GABAergic Neurogenesis in the Hippocampal CA1 Region of a Gerbil Model of Long-Term Survival after Transient Cerebral Ischemic Injury.Brain pathology (Zurich, Switzerland) · 2016Article
- Increases of Catalase and Glutathione Peroxidase Expressions by Lacosamide Pretreatment Contributes to Neuroprotection Against Experimentally Induced Transient Cerebral Ischemia.Neurochemical research · 2016Article
- Terminalia Chebula provides protection against dual modes of necroptotic and apoptotic cell death upon death receptor ligation.Scientific reports · 2016Article
- Mn-SOD Upregulation by Electroacupuncture Attenuates Ischemic Oxidative Damage via CB1R-Mediated STAT3 Phosphorylation.Molecular neurobiology · 2016Article
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fruit of Terminalia chebula Retz has been used as a traditional medicine in Asia and contains tannic acid, chebulagic acid, chebulinic acid and corilagin. Extract from T. chebula seeds (TCE) has various biological functions. We observed the neuroprotective effects of TCE against ischemic damage in the hippocampal C1 region (CA1) of the gerbil that had received oral administrations of TCE (100 mg/kg) once a day for 7 days before the induction of transient cerebral ischemia. In the TCE-treated ischemia group, neuronal neuclei (a marker for neurons)-positive neurons were distinctively abundant (62% of the sham group) in the CA1 4 days after ischemia-reperfusion (I-R) compared to those (12.2% of the sham group) in the vehicle-treated ischemia group. Four days after I-R TCE treatment markedly decreased the activation of astrocytes and microglia in the ischemic CA1 compared with the vehicle-treated ischemia group. In addition, immunoreactivities of Cu, Zn-superoxide dismutase (SOD1), Mn-superoxide dismutase (SOD2) and brain-derived neurotrophic factor (BDNF) in the CA1 of the TCE-treated ischemia group were much higher than those in the vehicle-ischemia group 4 days after I-R. Protein levels of SOD1, SOD2 and BDNF in the TCE-treated ischemia group were also much higher than those in the vehicle-ischemia group 4 days after I-R. These results indicate that the repeated supplement of TCE protected neurons from ischemic damage induced by transient cerebral ischemia by maintaining SODs and BDNF levels as well as decreasing glial activation.
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