| Literature DB >> 27087820 |
Byeong Cheol Yun1, Seung Bin Pae1, Yoo Kyoung Han1, Moo Jin Choi1, Byung Tae Choi2, Hwa Kyoung Shin2, Jin Ung Baek1.
Abstract
In contrast to Western medicine, which typically prescribes one medicine to treat a specific disease, traditional East Asian medicine uses any one of a large number of different prescriptions (mixtures of medicinal herbs), according to the patient's characteristics. Although this can be considered an advantage, the lack of a universal prescription for a specific disease is considered a drawback of traditional East Asian medicine. The establishment of universally applicable prescriptions for specific diseases is therefore required. As a basic first step in this process, this study aimed to select prescriptions used in the treatment of stroke and, through the analysis of medicinal herb combination frequencies, select a high-frequency medicinal herb combination group for further experimental and clinical research. As a result, we selected some candidates of a medicinal herb combination and 13 candidates of a medicinal herb for the treatment of stroke.Entities:
Year: 2016 PMID： 27087820 PMCID： PMC4818814 DOI： 10.1155/2016/2674014
Source DB: PubMed Journal: Evid Based Complement Alternat Med ISSN： 1741-427X Impact factor: 2.629
Medicinal herb combinations from 92 PTSs in the order of frequency (80%).
| Number of constituents | Name of constituents | Frequency |
|---|---|---|
| 1 | (1) | 15 |
| (2) | 15 | |
| (3) | 14 | |
| (4) | 12 | |
| (5) | 10 | |
| (6) | 10 | |
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| 2 | (1) | 9 |
| (2) | 8 | |
| (3) | 8 | |
| (4) | 7 | |
| (5) | 7 | |
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| 3 | (1) | 7 |
| (2) | 7 | |
| (3) | 6 | |
| (4) | 5 | |
| (5) | 5 | |
| (6) | 5 | |
| (7) | 5 | |
| (8) | 5 | |
| (9) | 5 | |
| (10) | 5 | |
| (11) | 5 | |
| (12) | 5 | |
| (13) | 5 | |
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| 4 | (1) | 5 |
| (2) | 5 | |
| (3) | 5 | |
| (4) | 5 | |
| (5) | 5 | |
| (6) | 5 | |
| (7) | 5 | |
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| 5 | (1) | 5 |
| (2) | 4 | |
| (3) | 4 | |
| (4) | 4 | |
| (5) | 4 | |
| (6) | 4 | |
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| 6 | (1) | 4 |
| (2) | 3 | |
| (3) | 3 | |
| (4) | 3 | |
| (5) | 3 | |
| (6) | 3 | |
| (7) | 3 | |
| (8) | 3 | |
| (9) | 3 | |
| (10) | 3 | |
| (11) | 3 | |
| (12) | 3 | |
| (13) | 3 | |
| (14) | 3 | |
| (15) | 3 | |
| (16) | 3 | |
| (17) | 3 | |
| (18) | 3 | |
| (19) | 3 | |
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| 7 | (1) | 3 |
| (2) | 3 | |
| (3) | 3 | |
Selecting CMHCTSs as the top 5 on the basis of frequency, only including frequencies greater than 3 and including ties for the 5th place.
Preliminary evaluation of the effects of 13 CMHTSs in stroke via analysis of the previous studies.
| Name of CMHTS | Classification of the study (number) | Source database/main outcome |
|---|---|---|
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| VT (2) | (1) P/attenuated A |
| (2) N and R/inhibited Glu-induced neurotoxicity with IC50 [ | ||
| VV (24) | (1) S/improved the outcome in rats after cerebral ischemia and reperfusion in terms of neurobehavioral function [ | |
| (2) P/improved the habituation memory, decreased AChE, corticosterone, and TNF- | ||
| (3) S/infarct volume of | ||
| (4) N/the expression of Ang-2 in the APS group was higher than that in the control group [ | ||
| (5) P, S, and N/the hyperintense signals and volume in the right cerebrum in | ||
| (6) N/the expression of VEGF in the | ||
| (7) P and N/increased the gene expression of Flt-1 and Flk-1 [ | ||
| (8) P, S, and N/reduced cerebral infarct and neurological deficit score and suppressed superoxide radicals in the parenchyma lesion [ | ||
| (9) P and R/prevented the decrease in the levels of phospho-Akt and phospho-GSK-3 | ||
| (10) P, S, and N/prevented neuronal loss, dendrites damage, and neuronal apoptosis in both parietal cortex and hippocampus of 2VO rats [ | ||
| (11) S and N/reduced brain swelling by 68.62% and 82.08% and significantly improved behavioral deficits [ | ||
| (12) N/inhibited cyclooxygenase-2 [ | ||
| (13) P, S, and N/decreased the level of malondialdehyde (MDA) and increased the activities of the antioxidant enzyme glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in the ischemic brain tissues [ | ||
| (14) P and S/reduced malondialdehyde levels and increased superoxide dismutase activity in ischemic brain tissue [ | ||
| (15) S/decreased the neurologic deficit score and the cerebral infarct volume rate [ | ||
| (16) P and S/reduced mortality, neurobehavioral deficits, brain edema, BBB permeability, and cerebral vasospasm [ | ||
| (17) P, S, and N/activated Nrf2/HO-1 pathway [ | ||
| (18) N and O/GFAP, CD81, and ERK of the brain in rats with cerebral infarction after MCAO were meaningfully decreased [ | ||
| (19) O and R/induced in infarction areas and volume [ | ||
| (20) N and O/elevated MCAO-induced decrease in density of neurons and c-Fos immunoreactive cells [ | ||
| (21) R/had neuroprotective effects via attenuation of COX-2 induction in hippocampus [ | ||
| (22) N, O, and R/inhibited decreasing the cell viability in ischemia-induced cells [ | ||
| (23) N, O, and R/reduced infarction volume in ischemic brains of rats, degradation of neuronal cell, BBB permeability, and expression of VEGF protein dose-dependently [ | ||
| (24) N and R/decreased infarction volume in ischemic brains and inhibited the expression of iNOS, Bax, and caspase-3 [ | ||
| C (1) | (1) P/decreased infarcted volume [ | |
| R (1) | (1) P/increased blood circulation and neuronal metabolism in an MCAO rat model [ | |
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| VV (1) | (1) O/change of brain bloodstream by preadministered Ds and Dn in cerebral ischemia and blood gas induction by MCAO did not appear [ |
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| Not available | |
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| VT (1) | (1) R/inhibited the hypoxia signaling pathway by reducing HIF-1a expression [ |
| VV (1) | (1) P/prevented growth inhibition, mitochondrial injury, and apoptosis of neurons induced by hypoxia [ | |
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| Not available | |
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| VT (2) | (1) S/prevented PC12 cell apoptosis in concentration-dependent manners [ |
| (2) P, S, and N/increased cAMP formation, PKA activity, and phosphorylation of the CREB protein [ | ||
| VV (13) | (1) P and S/decreased the infarct volume and edema volume and improved the neurological functions after MCAO [ | |
| (2) R/reduced infarction area in TTC stain and decreased necrosis in H&E stain [ | ||
| (3) R/showed lower modified neurological severity score (mNSS) [ | ||
| (4) P and S/attenuated the hippocampal neuronal damage in the CA1 region in high dose [ | ||
| (5) P and S/increased the levels of PDI (protein disulfide isomerase) and 1-Cys Prx (peroxiredoxin) transcription [ | ||
| (6) P, S, and N/increased the expression of Bcl-2 and inhibited the activation of caspase-3 ultimately inhibiting apoptosis [ | ||
| (7) P and S/expression of PDI, Nrf2, BDNF, GDNF, and MBP genes increased [ | ||
| (8) N and R/improved the neurological symptoms, reduced infarct volume and cerebral edema, and regulated the expression of CaMKII [ | ||
| (9) R/decreased infarct size in the brain of GEBs or 4-HBA group [ | ||
| (10) P and S/prevented hippocampal CA1 cell death following global ischemia [ | ||
| (11) O and R/had protective effects in the intraperitoneal injection of 1200 mg/kg and 600 mg/kg of Gastrodiae Rhizoma extracts [ | ||
| (12) O and R/reduced infarct size partly and volume significantly in the MCAO rat brain [ | ||
| (13) R/showed a significant decrease in infarct size in the ipsilateral brain with the extracts [ | ||
| R (3) | (1) S/had the greatest neuronal survival after ischemia insult with vanillin-treated animals [ | |
| (2) S/protected against neuronal cell damage after transient global ischemia in gerbils [ | ||
| (3) S/had correlation with stroke by statistics and association analysis [ | ||
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| VV (5) | (1) P, S, and N/had robust neuroprotection in the postischemic brain via anti-inflammatory effect by inhibiting HMGB1 phosphorylation and secretion [ |
| (2) P, S, and N/decreased the focal infarct volume, cerebral histological damage, and apoptosis in MCAO rats [ | ||
| (3) P, S, and N/the neurological deficits, infarct volume, and the levels of MDA and carbonyl decreased [ | ||
| (4) P/reduced LDH release from PC12 cells exposed to hypoxic chamber [ | ||
| (5) P, S, and N/inhibited the increases of brain MDA content and prevented the activities of brain superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) from decline caused by cerebral ischemia-reperfusion [ | ||
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| VT (6) | (1) N/the levels of tumor necrosis factor- |
| (2) P, S, and N/reduced cerebral infarct and neurological deficit score [ | ||
| (3) P and R/prevented the decrease in the levels of phospho-Akt and phospho-GSK-3 | ||
| (4) P, S, N, and R/decreased the infarct size and behavior deficits score [ | ||
| (5) N/scores of neurological deficit and infarct volume were lower significantly in the groups treated with volatile oil, and the nitric oxide (NO) and malondialdehyde (MDA) levels were found to be decreased [ | ||
| (6) O and R/reduced the infarction areas and volume [ | ||
| C (3) | (1) N/results are healing in 19 cases, obvious effect in 13 cases, availability in 5 cases, and invalidation in 3 cases; healing and obvious effect rate: 80.0% [ | |
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| VV (14) | (1) P/ischemia-reperfusion significantly increased AUC values, decreased CL values, and prolonged the terminal half-life of paeoniflorin [ |
| (2) P/prevented reduction of Na(+)-K(+)-ATPase activity, increased NO level, and enhanced NOS activity [ | ||
| (3) P and S/reduced the infarct volume and alleviated related tongue protrusion (TP) [ | ||
| (4) S, N, and R/the injuries of ischemia-reperfusion could play an important role in pharmacokinetic process of paeoniflorin in the cortex after intravenous administration of Paeoniae Radix extract [ | ||
| (5) P/displaced the binding of [3H]NECA to the membrane preparation of rat cerebral cortex in a manner different from its classical agonists [ | ||
| (6) P and S/reduced protein levels of Ras, MEK, p-MEK, and p-ERK [ | ||
| (7) P and S/produced delayed protection in the ischemia-injured rats via inhibiting MAPKs/NF- | ||
| (8) P/increased cell survival rate and reduced the binding activity of NMDA receptors [ | ||
| (9) P/inhibited | ||
| (10) P and S/reduced the cerebral infarction area and the neurodeficit score and reduced lucigenin-CL counts at 2 h period of reperfusion [ | ||
| (11) P/reduced the decrease of superoxide dismutase (SOD), inhibited the increase of nitric oxide (NO), and lessened the level of malondialdehyde (MDA) and reduced the decrease of lactate dehydrogenase (LDH) in cerebrum remarkably [ | ||
| (12) P/relieved brain edema, enhanced SOD activity, and lowered MDA concentration in the gerbils and had milder injury of the cells in the hippocampal CA1 region [ | ||
| (13) P/prolonged gasp time of decapitative mice, lessened cerebral water content, and decreased permeability of cerebral capillary [ | ||
| (14) P, S, and N/reduced the counts of ED1, IL-1beta, TNF-alpha, and ICAM-1 of microvessels and MPO immunoreactive cells and apoptotic cells [ | ||
| R (1) | (1) S/showed less potent caspase inhibitory activity [ | |
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| Not available | |
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| VV (1) | (1) N/showed neuroprotective effects with EC50 values of 21.6 |
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| VT (1) | (1) P, S, and N/increased astrocyte survival significantly in a concentration-dependent manner [ |
| VV (3) | (1) P and S/enhanced angiogenesis around the infarct of cortex and neurogenesis in the hippocampal dentate gyrus (DG) [ | |
| (2) P, S, and N/rescued neurons in hippocampal CA1 subfield and reduced working errors during behavioral testing [ | ||
| (3) S and N/upregulated GAP-43 protein expression [ | ||
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| VT (1) | (1) P, S, and N/did not block NMDA-induced neuronal death [ |
| VV (20) | (1) P, S, and N/activated GABAergic signaling and HSP70 and MAPKs cascades in global ischemia [ | |
| (2) P, S, and N/performed well in regulating proteins in energy metabolism but had a relatively weak effect in the regulation of proteins in neurogenesis and apoptosis [ | ||
| (3) P, S, and N/the level of NF- | ||
| (4) P, S, and N/suppressed caspase-3 in ischemic gerbils hippocampus [ | ||
| (5) P, S, and N/inhibited the formation of 3-nitrotyrosine, reduced infarct size, and attenuated apoptotic cell death, whose effects were similar to FeTMPyP [ | ||
| (6) P, S, N, and R/inhibited microglial tumor necrosis factor-alpha (TNF-alpha) and nitric oxide production [ | ||
| (7) P, S, N, and R/the increased contents of MDA and NO and SOD activity and the decreased activity of CAT in the hippocampus and cerebral cortex induced by cerebral ischemia were differently reversed [ | ||
| (8) P, S, and N/the activities of lactate dehydrogenase, Na(+)-K(+)-ATPase, Ca(2+)-ATPase, and superoxide dismutase were significantly lowered [ | ||
| (9) P/increased cell survival and inhibited cell apoptosis and excessive production of malondialdehyde [ | ||
| (10) R/decreased the release of neuron-specific enolase and the production of TBARS [ | ||
| (11) N/reduced the volume of infarction in the cerebral cortex as well as in the striatum [ | ||
| (12) P, S, N, and R/reduced the infarct volume, prevented apoptosis in hippocampal cells, attenuated neuronal and blood-brain barrier damage, and upregulated Bcl-2 protein expression [ | ||
| (13) P and S/reduced brain water content and the permeability of blood vessels, ameliorated ischemia-induced morphology changes in hippocampal microvessels, and downregulated Fas and FasL protein expression [ | ||
| (14) P, S, N, and R/prolonged gasping time (prolonged ratio: 23.79%) and survival time after carotid artery occlusion and decreased malondialdehyde (MDA) content in damaged brain tissues [ | ||
| (15) P and S/inhibited PKC(alpha) translocation [ | ||
| (16) N/protected CA1 hippocampal neurons against 20 min transient forebrain ischemia [ | ||
| (17) P, S, and N/attenuated neuronal injury and improved abnormality of energy metabolites in rats induced by global ischemia [ | ||
| (18) P and S/inhibited MMP-9 activity in the hippocampus [ | ||
| (19) O/CAT and GSH were activated by Scutellaria Radix extract administration [ | ||
| (20) P, S, and N/reduced the pMCAO- (permanent occlusion of middle cerebral artery-) induced infarct areas in the cerebral cortex as well as in the striatum [ | ||
| R (2) | (1) S/exerted neuroprotection by inhibiting TNF- | |
| (2) P/Had antiapoptotic and antiglutamate activity which are the key processes for neuroprotection [ | ||
PubMed (P), Cochrane (C), Scopus (S), Ndsl (N), Oasis (O), and Riss (R)
In vitro study (VT), in vivo study (VV), clinical study (C), and review (R).