Pretreatment of Populus tomentiglandulosa protects hippocampal CA1 pyramidal neurons from ischemia-reperfusion injury in gerbils via increasing SODs expressions and maintaining BDNF and IGF-I expressions / 中国天然药物
Chinese Journal of Natural Medicines (English Ed.)
; (6): 424-434, 2019.
Article
de En
| WPRIM
| ID: wpr-776868
Bibliothèque responsable:
WPRO
ABSTRACT
To examine the effects of Populus tomentiglandulosa (PT) extract on the expressions of antioxidant enzymes and neurotrophic factors in the cornu ammonis 1 (CA1) region of the hippocampus at 5 min after inducing transient global cerebral ischemia (TGCI) in gerbils, TGCI was induced by occlusion of common carotid arteries for 5 min. Before ischemic surgery, 200 mg·kg PT extract was orally administrated once daily for 7 d. We performed neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B staining. Furthermore, we determined in situ production of superoxide anion radical, expression levels of SOD1 and SOD2 as antioxidant enzymes and brain-derived neurotrophic factor (BDNF) and insulin-like growth factor I (IGF-I) as neurotrophic factors. Pretreatment with 200 mg·kg PT extract prevented neuronal death (loss). Furthermore, pretreatment with 200 mg·kg PT extract significantly inhibited the production of superoxide anion radical, increased expressions of SODs and maintained expressions of BDNF and IGF-I. Such increased expressions of SODs were maintained in the neurons after IRI. In summary, pretreated PT extract can significantly increase levels of SODs and protect the neurons against TGCI, suggesting that PT can be a useful natural agent to protect against TGCI.
Mots clés
Texte intégral:
1
Indice:
WPRIM
Sujet Principal:
Superoxide dismutase
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Facteur de croissance IGF-I
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Extraits de plantes
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Lésion d'ischémie-reperfusion
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Régulation positive
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Chimie
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Gerbillinae
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Cellules pyramidales
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Neuroprotecteurs
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Facteur neurotrophique dérivé du cerveau
Limites du sujet:
Animals
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Humans
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Male
langue:
En
Texte intégral:
Chinese Journal of Natural Medicines (English Ed.)
Année:
2019
Type:
Article