Chinese medicine Nao-Shuan-Tong attenuates cerebral ischemic injury by inhibiting apoptosis in a rat model of stroke

Xiang, Jun; Tang, Yuping; Wu, Ping; Gao, Jiantou; Cai, Dingfang

doi:10.1016/j.jep.2010.06.021

Cited by 30 publications

(11 citation statements)

References 32 publications

(33 reference statements)

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“…Based on the theory of TCM, together with modern pharmacological knowledge of herbal medicines, a neuroprotective formula called Post-Stroke Rehabilitation (PSR), comprising seven herbs (Table 1) has been designed. Most chosen herbs have been used in herbal mixtures for stroke treatment, including Buyang Huanwu, Sheng Yu, Xiaoxuming, Gualou Guizhi and Wen Dan Decoctions as well as BNG-1, Hua Tan Tong Luo formula and Nao-Shuan-Tong [22–30]. Moreover, extracts and/or isolates from all constituent herbs have been demonstrated to be neuroprotective in cell and/or animal models.…”

Section: Introductionmentioning

confidence: 99%

“…Paeonia lactiflora Pall. (Chishao)A component of BYHWD [22] and Nao-Shuan-Tong [30]; showed proliferative effects on injured rat peripheral neurons and Schwann cells [31, 32] ; an isolate, paeoniflorin, was neuroprotective in cerebral ischemic rats [86]4. Cassia obtusifolia L. (Juemingzi)Used for hyperlipidemia treatment [44]; showed neuroprotective effects in hippocampal neurons and in cell and animal models of Parkinson’s disease in mice [33, 34] ; an isolate, chrysophanol, showed neuroprotective effect in ischemic mice [87]5.…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotective effect of a novel Chinese herbal decoction on cultured neurons and cerebral ischemic rats

Zhao

Chan

et al. 2016

BMC Complement Altern Med

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BackgroundHistorically, traditional Chinese medicine has been widely used to treat stroke. Based on the theory of Chinese medicine and the modern pharmacological knowledge of herbal medicines, we have designed a neuroprotective formula called Post-Stroke Rehabilitation (PSR), comprising seven herbs – Astragalus membranaceus (Fisch.) Bunge, Salvia miltiorrhiza Bunge, Paeonia lactiflora Pall., Cassia obtusifolia L., Ligusticum chuanxiong Hort., Angelica sinensis (Oliv.) Diels, and Glycyrrhiza uralensis Fisch. We aim to examine the neuroprotective activity of PSR in vitro and in vivo, and to explore the underlying molecular mechanisms, to better understand its therapeutic effect and to further optimize its efficacy.MethodsPSR extract or vehicle was applied to primary rat neurons to examine their survival effects against N-methyl-d-aspartate (NMDA)-elicited excitotoxicity. Whole-cell patch-clamp recording was conducted to examine the NMDA-induced current in the presence of PSR. ERK- and CREB-activation were revealed by western blot analysis. Furthermore, PSR was tested for CRE promoter activation in neurons transfected with a luciferase reporter. The protective effect of PSR was then studied in the rat middle cerebral artery occlusion (MCAO) model. MCAO rats were either treated with PSR extract or vehicle, and their neurobehavioral deficit and cerebral infarct were evaluated. Statistical differences were analyzed by ANOVA or t-test.ResultsPSR prominently reduced the death of cultured neurons caused by NMDA excitotoxicity in a dose-dependent manner, indicating its neuroprotective property. Furthermore, PSR significantly reduced NMDA-evoked current reversibly and activated phosphorylation of ERK and CREB with distinct time courses, with the latter’s kinetics slower. PSR also triggered CRE-promoter activity as revealed by the increased expression of luciferase reporter in transfected neurons. PSR effectively reduced cerebral infarct and deficit in neurological behavior in MCAO rats when PSR decoction was administered starting either 6 days before or 6 h after onset of ischemia.ConclusionsPSR is neuroprotective both in vitro and in vivo – it protects cultured neurons against NMDA excitotoxicity, and effectively reduces ischemic injury and neurobehavioral deficit in MCAO rats in both the pre- and post-treatment regimens. The underlying neuroprotective mechanisms may involve inhibition of NMDA receptor current and activation of ERK and CREB. This study provides important preclinical data necessary for the further development of PSR for stroke treatment.Electronic supplementary materialThe online version of this article (doi:10.1186/s12906-016-1417-1) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neuroprotective effect of a novel Chinese herbal decoction on cultured neurons and cerebral ischemic rats

Zhao

Chan

et al. 2016

BMC Complement Altern Med

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“…Ischemic stroke results from a temporary or permanent reduction of cerebral blood flow that leads to functional and structural damage in different brain regions. Cellular damage occurs during ischemia [ 3 , 4 ] and reperfusion [ 5 , 6 ]. Despite decades of intense research, the beneficial treatment of stroke remains limited [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

The protective effect of caffeic acid on global cerebral ischemia-reperfusion injury in rats

et al. 2015

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Ischemic stroke is a major cause of death and disability all over the world. Ischemic stroke results from a temporary or permanent reduction of cerebral blood flow that leads to functional and structural damage in different brain regions. Despite decades of intense research, the beneficial treatment of stroke remains limited. In light of this, the search for effective means ameliorating cerebral ischemia-reperfusion injury (CIRI) is one of the major problems of experimental medicine and biology. Recently, the 5-Lipoxygenase (5-LO, a key enzyme metabolizing arachidonic acid to produce leukotrienes) inhibitors have been showed to protect brain against ischemic damage in animal model of cerebral ischemia. Caffeic acid, an inhibitor of 5-LO, is a phenolic compound widely distributed in medicinal plants. The aim of this study was to investigate the effect of caffeic acid on global cerebral ischemia-reperfusion injury in rats. The study was carried out on 45 rats that were randomly divided into five groups: the sham group (n = 9), I/R non-treated group (n = 9), I/R-caffeic acid group (10 mg · kg−1) (n = 9), I/R-caffeic acid group (30 mg · kg−1) (n = 9) and I/R-caffeic acid group (50 mg · kg−1) (n = 9). Global cerebral ischemia was induced by bilateral carotid artery occlusion for 20 min followed by reperfusion. Spatial learning and memory was evaluated using Morris water maze. Histopathological changes of hippocampus neurons was observed using HE staining. Superoxide dismutase (SOD, the antioxidant enzyme) activities and malondialdehyde (MDA, an oxidative stress biomarker) contents were detected. NF-κBp65 expression was detected by the methods of immunohistochemistry. Caffeic acid markedly reduced the escape latency, relieved hippocampal neurons injury and increased neuron count compared with those of I/R non-treated rat. NF-κBp65 expression and MDA content decreased significantly, and SOD activities increased significantly in hippocampus. Compared with sham group, 5-LO expression increase significantly in I/R non-treated group rat, and caffeic acid markedly reduced 5-LO expression. The results of the study suggest that caffeic acid has a significant protective effect on global cerebral ischemia-reperfusion injury in rats. The neuroprotective effects is likely to be mediated through the inhibition of 5-LO.

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“…Cellular damage occurs during ischemia [1, 2] and reperfusion [3, 4]. Deleterious effects include ATP depletion, intracellular calcium changes, loss of ion homeostasis, excitotoxicity, activation of enzymes, arachidonic acid release, and mitochondrial dysfunction [5, 6].…”

Section: Introductionmentioning

confidence: 99%

Green Tea Extract Ameliorates Learning and Memory Deficits in Ischemic Rats via Its Active Component Polyphenol Epigallocatechin-3-gallate by Modulation of Oxidative Stress and Neuroinflammation

Hsieh

et al. 2012

Evidence-Based Complementary and Alternative Medicine

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Ischemic stroke results in brain damage and behavioral deficits including memory impairment. Protective effects of green tea extract (GTex) and its major functional polyphenol (−)-epigallocatechin gallate (EGCG) on memory were examined in cerebral ischemic rats. GTex and EGCG were administered 1 hr before middle cerebral artery ligation in rats. GTex, EGCG, and pentoxifylline (PTX) significantly improved ishemic-induced memory impairment in a Morris water maze test. Malondialdehyde (MDA) levels, glutathione (GSH), and superoxide dismutase (SOD) activity in the cerebral cortex and hippocampus were increased by long-term treatment with GTex and EGCG. Both compounds were also associated with reduced cerebral infraction breakdown of MDA and GSH in the hippocampus. In in vitro experiments, EGCG had anti-inflammatory effects in BV-2 microglia cells. EGCG inhibited lipopolysaccharide- (LPS-) induced nitric oxide production and reduced cyclooxygenase-2 and inducible nitric oxide synthase expression in BV-2 cells. GTex and its active polyphenol EGCG improved learning and memory deficits in a cerebral ischemia animal model and such protection may be due to the reduction of oxidative stress and neuroinflammation.

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Chinese medicine Nao-Shuan-Tong attenuates cerebral ischemic injury by inhibiting apoptosis in a rat model of stroke

Cited by 30 publications

References 32 publications

Neuroprotective effect of a novel Chinese herbal decoction on cultured neurons and cerebral ischemic rats

Neuroprotective effect of a novel Chinese herbal decoction on cultured neurons and cerebral ischemic rats

The protective effect of caffeic acid on global cerebral ischemia-reperfusion injury in rats

Green Tea Extract Ameliorates Learning and Memory Deficits in Ischemic Rats via Its Active Component Polyphenol Epigallocatechin-3-gallate by Modulation of Oxidative Stress and Neuroinflammation

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