Study on effect of weinaokang and bilobalide on autophagy and neurogenesis induced by focal cerebral ischemia reperfusion.
- Author:
Yong-Qiu ZHENG
1
;
Jian-Xun LIU
;
Li XU
;
Ming-Jiang YAO
;
Wen-Ting SONG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Autophagy; drug effects; Brain Ischemia; drug therapy; pathology; physiopathology; Cyclopentanes; pharmacology; Drugs, Chinese Herbal; pharmacology; Furans; pharmacology; Ginkgolides; pharmacology; Male; Neurogenesis; drug effects; Neurons; ultrastructure; Rats; Rats, Sprague-Dawley; Reperfusion Injury; prevention & control
- From: China Journal of Chinese Materia Medica 2013;38(13):2182-2186
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the protective effect of the Weinaokang (WNK) and its active compound bilobalide on focal cerebral ischemia reperfusion, and their mechanisms.
METHODThe 60-minute middle cerebral artery occlusion (MCAO) was adopted to establish the 24 h-14 d reperfusion model. The expression of Beclin-1 was detected by the Western blotting technique. The transmission electron microscopy was used to observe ultrastructural changes. Neurogenesis was detected by the immunofluorescence staining.
RESULTWNK (20, 10 mg x kg(-1), ig) or its active compound bilobalide (10, 5 mg x kg(-1), ig) could promote the generation of mature neurons (BrdU(+) -MAP-2+) at the ischemic side, and inhibit expression of autophagy-related gene Beclin-1, so as to reduce the neuron injury induced by focal cerebral ischemia reperfusion.
CONCLUSIONWNK and its active compound bilobalide can inhibit neuron autophagy and improve neurogenesis in ischemic peripheral area, suggesting that neurogenesis may be the intervention target for WNK to promote self-repairing of ischemic area.
