Neuroprotective effects of a standardized flavonoid extract from Diospyros kaki leaves

被引：74

作者：

Bei, Weijian ^{[1
]}

Zang, Linquan ^{[2
]}

Guo, Jiao ^{[1
]}

Peng, Wenlie ^{[3
]}

Xu, Anlong ^{[3
]}

Good, David A. ^{[4
]}

Hu, Yinming ^{[1
]}

Wu, Wei ^{[2
]}

Hu, Dehui ^{[5
]}

Zhu, Xinghong ^{[5
]}

Wei, Ming ^{[4
]}

Li, Chuyuan ^{[6
]}

机构：

[1] Guangdong Pharmaceut Univ, Inst Chinese Med Sci, Guangzhou Higher Educ Mega Ctr, Guangzhou 510006, Guangdong, Peoples R China

[2] Guangdong Pharmaceut Univ, Dept Pharmacol, Guangzhou Higher Educ Mega Ctr, Sch Pharm, Guangzhou 510006, Guangdong, Peoples R China

[3] Sun Yat Sen Univ, Sch Life Sci, Key Lab Genet Engn MOE, Guangzhou 510275, Guangdong, Peoples R China

[4] Griffith Univ, Sch Med Sci, Div Mol & Gene Therapies, Griffith, Qld 4222, Australia

[5] Nanfang Med Univ, Dept Physiol, Guangzhou 510515, Guangdong, Peoples R China

[6] Hutchison Whampoa Guangzhou Baiyunshan Chinese Me, Inst Modern TCM, Guangzhou, Guangdong, Peoples R China

来源：

JOURNAL OF ETHNOPHARMACOLOGY | 2009年 / 126卷 / 01期

关键词：

Flavonoid; Diospyros kaki leaves; Central nervous system; Pharmacology; Neuroprotection; Middle cerebral artery occlusion; Ischemia; Reperfusion; Hypoxia; PEROXIDE-INDUCED INJURY; HYDROGEN-PEROXIDE; CULTURED NEURONS; OXIDATIVE STRESS; CELL-CULTURE; GLUTAMATE; DEATH; BCL-2; ANTIOXIDANTS; MECHANISMS;

D O I：

10.1016/j.jep.2009.07.034

中图分类号：

Q94 [植物学];

学科分类号：

071001 [植物学];

摘要：

Ethnopharmacological relevance: Flavonoids, extracted from the leaves of Diospyros kaki, are the main therapeutic components of NaoXingQing (NXQ), a potent and patented Chinese herbal remedy widely used in China for the treatment of apoplexy syndrome. Aim of the study: To investigate the neuroprotective effects of FLDK-P70, a standardized flavonoid extract, using ill vivo rat models of both focal ischemia/reperfusion (I/R) injury induced by middle cerebral artery occlusion (MCAO) and oil transient global brain ischemia induced by four-vessel occlusion (4-VO). We also aim to examine the effects of FLDK-P70 Oil glutamate-induced cell injury of hippocampal neurons as well as oil hypoxia-induced injury of cortical neurons in primary cell Culture. Materials and methods and results: Administration of FLDK-P70 for 12 days (40, 80 mg/kg body weight, p.o., 5 days before and 7 days after 4-VO) increased the survival of hippocampal CA1 pyramidal neutrons after transient global brain ischemia. Similarly, administration of FLDK-P70 for 7 days (40,80 mg/kg body weight, p.o., 3 days before and 4 days after MCAO) significantly reduced the lesion of the insulted brain hemisphere and improved the neurological behavior of rats. In primary rat hippocampal neuronal cultures, pretreatment with FLDK-P70 (5, 10 mu g/ml) protected neurons from glutamate-induced excitotoxic neuronal death in a dose-dependent manner. In primary rat cerebral cortical neuronal culture. pretreatment with FLDK-P70 (25, 100 mu g/ml) also reduced hypoxia-reoxygen induced neuronal death and apoptosis in a dose-dependent manner. Conclusions:These in vivo and in vitro results suggest that FLDK-P70 significantly Protects rats from MCAO and 4-VO ischemic injury in vivo and protects hippocampal neurons from glutamate-induced excitotoxic injury as well as cortical neurons from hypoxia-induced injury in vitro. The mechanisms of these effects may be due to the antioxidative activity of the flavonoids. These results convincingly demonstrate that FLDK-P70 may be useful for the prevention and treatment of ischemia/reperfusion injury and other related neurodegenerative diseases. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

引用

页码：134 / 142

页数：9

共 43 条

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CHELATING AND FREE-RADICAL SCAVENGING MECHANISMS OF INHIBITORY-ACTION OF RUTIN AND QUERCETIN IN LIPID-PEROXIDATION [J].