Angelica sinensis extract protects against ischemia-reperfusion injury in the hippocampus by activating p38 MAPK-mediated p90RSK/p-Bad and p90RSK/CREB/BDNF signaling after transient global cerebral ischemia in rats

被引:42
|
作者
Cheng, Chin-Yi [1 ,2 ]
Kao, Shung-Te [3 ]
Lee, Yu-Chen [4 ,5 ,6 ]
机构
[1] China Med Univ, Coll Chinese Med, Sch Postbaccalaureate Chinese Med, Taichung 40402, Taiwan
[2] Hui Sheng Hosp, Dept Chinese Med, Taichung 42056, Taiwan
[3] China Med Univ, Coll Chinese Med, Sch Chinese Med, Taichung 40402, Taiwan
[4] China Med Univ Hosp, Dept Chinese Med, Taichung 40447, Taiwan
[5] China Med Univ, Res Ctr Chinese Med & Acupuncture, Taichung 40402, Taiwan
[6] China Med Univ, Grad Inst Acupuncture Sci, 91 Hsueh Shih Rd, Taichung 40402, Taiwan
关键词
Global cerebral ischemia; Angelica sinensis; p38 mitogen-activated protein kinase; 90-kDa ribosomal S6 kinase; Phospho-Bad; Brain-derived neurotrophic factor; INDUCED MEMORY IMPAIRMENT; PERMEABILITY TRANSITION; NEURONAL APOPTOSIS; INDUCED DECREASE; GENE-EXPRESSION; BRAIN-DAMAGE; DEFICITS; PATHWAY; MODEL; NEUROPROTECTION;
D O I
10.1016/j.jep.2020.112612
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Ethnopharmacological relevance: Angelica sinensis (Oliv.) Diels, commonly known as Dang Gui (DG), is one of the most popular traditional Chinese herbal medicines for the treatment of stroke. However, the effects of DG on transient global cerebral ischemia (GCI) and its precise mechanisms remain unclear. Aim of the study: This study aimed to investigate the effects of the DG extract on ischemia-reperfusion (I/R) injury in the hippocampus 7 d after transient GCI and to identify the potential mitogen-activated protein kinase (MAPK)-related signaling pathway in the hippocampus involved in the effects. Materials and methods: Rats were intragastrically administered DG at doses of 0.25 g/kg (DG-0.25g), 0.5 g/kg (DG-0.5g), or 1 g/kg (DG-1g) 1, 3, and 5 d after GCI. Results: DG-0.5g and DG-1g treatments effectively promoted hippocampal cornu ammonis 1 (CA1) neuronal survival. DG-0.5g and DG-1g treatments markedly increased phospho-p38 MAPK (p-p38 MAPK), phospho-90-kDa ribosomal S6 kinase (p-p90RSK), cytosolic and mitochondrial phospho-Bad (p-Bad), phospho-cAMP response element-binding protein (p-CREB), brain-derived neurotrophic factor (BDNF), and p-CREB/BDNF expression; decreased 4-hydroxy-2-nonenal, cytochrome c (Cytc), and cleaved caspase-3 expression, and inhibited apoptosis in the hippocampal CA1 region. Pretreatment with a specific inhibitor of p38 MAPK, SB203580, completely blocked the effects of DG-1g on the expression of the aforementioned proteins. Conclusions: DG-0.5g and DG-1g treatments exerted neuroprotective effects on I/R injury by activating p38 MAPK-mediated p90RSK/p-Bad-induced anti-apoptotic-Cytc/caspase-3-related and p90RSK/CREB/BDNF survival signaling in the hippocampus 7 d after transient GCI.
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收藏
页数:14
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