Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Shenshao Tongguan Pian (SSTGP) is composed chiefly of saponins from the stem and leaf of Ginseng and Radix Paeoniae Alba, etc. The authors applied this remedy for the treatment of angina pectoris of CHD. From 1982-1988, the authors carried out a randomized double blind trial on altogether 565 cases of CHD divided into an experimental group to be treated with SSTGP and a control group treated with another TCM proprietory medicine, Dan Qi Pian, that had been used for many years clinically. The total effective rate of treating angina pectoris was 94.71% and ECG improvement rate 63.38% in experimental group whereas 66.99% and 23.38% respectively in the control group, the difference being very significant (P less than 0.01). Experiments with animals proved that SSTGP had more potent actions on CV system, such as dilatation of coronary arteries, promotion of coronary perfusion flow, lowering oxygen consumption of heart muscle, resisting the coronary spasm, anoxia and ischemia of heart muscle elicited by pituitrin, and prolongation of survival time of mice under anoxic state. In addition, laboratory examination also revealed SSTGP could promote the left ventricular output, lower the blood viscosity and inhibit the aggregation of blood platelets. Both acute and chronic toxicity tests showed SSTGP has no toxicity nor side effects. Therefore SSTGP is a new, safe and effective TCM proprietory remedy for CHD and angina pectoris.
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PMID:[Clinical and experimental study of shenshao tongguan pian in treating angina pectoris of coronary heart disease]. 226 17

Sheng-Mai-San (SMS), a traditional Chinese formulation used for the treatment of coronary heart disease, is comprised of Radix Ginseng, Fructus Schisandrae and Radix Ophiopogonis. Pretreatment with a lignan-enriched SMS (17 g/kg/day x 3, p.o.) was found effective in protection against isoproterenol-induced myocardial injury in rats, and in ischemia-reperfusion injury in isolated perfused hearts prepared from pretreated animals. Results obtained from pretreatment studies using extracts prepared by mixing various combinations of the three component herbs indicate that the major myocardial protective component in SMS is the lignan-enriched extract of Fructus Schisandrae.
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PMID:Schisandra chinensis-dependent myocardial protective action of sheng-mai-san in rats. 898 37

The protective activity of Shengmai San, a traditional Chinese herbal medicine, was studied in cerebral ischemia-reperfusion injury in rats. Shengmai San consists of three herbal components, Panax Ginseng, Ophiopogon Japonicus and Schisandra Chinensis and is routinely being used for treating coronary heart disease. When Shengmai San was injected directly into rat duodenum 2h before cerebral ischemia by bilateral carotid artery occlusion, thiobarbituric acid reactive substance (TBARS) formation during reperfusion following ischemia was almost completely suppressed in the brain. The loss of glutathione peroxidase activity after the ischemia-reperfusion was also effectively prevented by the Shengmai San pre-administration whereas the activity was considerably decreased in the damaged brain. It was found that Shengmai San also effectively suppressed the TBARS formation even when it was administered after 45 min reperfusion following ischemia, indicating that Shengmai San improves the oxidative damage already established in the brain. Likewise, the decrease of glutathione peroxidase activity was minimized in the damaged brain by the post-administration of Shengmai San. On the other hand, none of the Shengmai San components were active in protecting the ischemia-reperfusion brain damage when they were independently administered. These experiments suggest the potential of Shengmai San in both preventive and therapeutic usages for cerebral ischemia-reperfusion injury.
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PMID:Prevention and repair of cerebral ischemia-reperfusion injury by Chinese herbal medicine, shengmai san, in rats. 1054 89

The present study used isolated rat hearts to investigate whether (1) Sheng-Mei-San (SMS), a traditional Chinese formulation comprising Radix Ginseng, Radix Ophiopogonis and Fructus Schisandrae, is protective against post-ischemic myocardial dysfunction, and (2) whether the cardioprotective effect of SMS is related to scavenging of hydroxyl radicals and opening the mitochondrial KATP channels. The excised hearts of male Sprague-Dawley rats were perfused on a Langendorff apparatus with Krebs-Henseleit solution with a gas mixture of 95% O2 and 5% CO2. Left ventricular end-diastolic pressure (LVEDP, mmHg), left ventricular developed pressure (LVDP, mmHg), +/-dP/dt (mmHg/s) and coronary flow (ml/min) were continuously monitored. All hearts were perfused for a total of 120 min consisting of a 30-min pre-ischemic period followed by a 30-min global ischemia and 60-min reperfusion. Lactate, lactate dehydrogenase (LDH) and 2,5-dihydroxybenzoic acid (2,5-DHBA) concentrations in the effluent were measured during reperfusion. Three days' treatment with SMS (1.67 ml/kg per day) inhibited the rise in LVEDP and improved the post-ischemic LVDP and +/-dP/dt significantly better than in the untreated control hearts during reperfusion. SMS increased the coronary flow at baseline, and during reperfusion. Pretreatment with 5-hydroxydecanoic acid (5-HD), a mitochondrial KATP channel blocker, abolished the inhibition of the rise in LVEDP, the increase in coronary flow and the improvement in LVDP and +/-dP/dt induced by SMS. SMS significantly attenuated the concentrations of lactate, LDH and 2,5-DHBA during reperfusion, but the pretreatment with 5-HD restored them; 5-HD alone did not affect the concentrations. SMS improved the post-ischemic myocardial dysfunction through opening the mitochondrial KATP channels.
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PMID:Sheng-Mai-San is protective against post-ischemic myocardial dysfunction in rats through its opening of the mitochondrial KATP channels. 1219 3

Ginseng was incubated under mildly acidic conditions and its inhibitory effect on a rat ischemia-reperfusion model was investigated. When ginseng was treated with 0.1% hydrochloric acid at 60 degrees C, its protopanaxadiol saponins were transformed to diasteromeric ginsenoside Rg3 and Delta20-ginsenoside Rg3. When the transformed ginseng extract, of which the main component was ginsenosides Rg3, was treated with human intestinal microflora, the main metabolite was ginsenoside Rh2. Orally administered acid-treated ginseng (AG) extract and ginsenoside Rh2 potently protect ischemia-reperfusion brain injury. The ginsenoside Rh2 also inhibited prostaglandin-E2 synthesis in lipopolysaccharide-stimulated RAW264.7 cells, but showed no in vitro antioxidant activity. These results suggest that AG and ginsenoside Rh2 can improve ischemic brain injury.
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PMID:Ginsenoside Rh2 reduces ischemic brain injury in rats. 1499 18

The present study used in vivo rat heart to investigate (1) whether Shen-Fu (SF), a traditional Chinese formulation comprising Radix Ginseng (RG) and Radix Aconitum Carmichaeli (AC), is protective against myocardium damage due to ischemia-reperfusion injury, and (2) whether the cardioprotective effect of SF is related to scavenging of hydroxyl radicals. The model of ischemia-reperfusion injury was established by ligation of left anterior descending coronary artery for 60 minutes followed by reperfusion for 240 minutes in anesthetized rats. The size of infarction and the pathologic changes of myocardium were observed. Lactate dehydrogenase (LDH) and creatine kinase (CK) in serum, the amounts of malondialdehyde (MDA) and superoxide dismutase (SOD) in myocardium were measured at the end of the reperfusion period. Pretreatment groups with SF (10 mg/kg), RG (9 mg/kg) and AC (1 mg/kg) inhibited the rise in MDA and LDH as well as CK, increased SOD activity, reduced the size of infarction, and improved the pathologic changes of myocardium during ischemia-reperfusion compared with the control group. The effect of SF is better than that of RG and AC. These results indicate that SF, RG and AC protect obviously myocardium against damage due to ischemia-reperfusion in rats. The cardioprotective effect of SF injection may be in part related to scavenging of hydroxyl radicals or inhibition of lipid peroxidation. SF is more effective than its separated herbal extracts prepared from RG and AC.
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PMID:Protective effect of shen-fu on myocardial ischemia-reperfusion injury in rats. 1531 59

Ameliorating effects of ginseng were observed on neuronal cell death associated with ischemia or glutamate toxicity. Ginseng saponins are transformed by intestinal microflora and the transformants would be absorbed from intestine. In the present study, we have investigated the effects of transformed ginsenoside Rg3, Rh2 and compound K on the modulation of NMDA receptor and GABAA receptor binding in rat brain. The NMDA receptor binding was analyzed by quantitative autoradiography using [3H]MK-801 binding, and GABAA receptor bindings were analyzed by using [3H]muscimol and [3H]flunitrazepam binding in rat brain slices. Ginsenoside Rg3, Rh2 and compound K were infused (10 microg/10 microl/h) into rat brain lateral ventricle for 7 days, through pre-implanted cannula by osmotic minipumps (Alzet, model 2ML). The levels of [3H]MK-801 binding were highly decreased in almost all regions of frontal cortex and hippocampus by ginsenoside Rh2 and compound K. The levels of [3H]muscimol binding were elevated in part of frontal cortex and granule layer of cerebellum by the treatment of ginsenoside Rh2 and compound K. However, the [3H]flunitrazepam binding was not modulated by any tested ginsenosides. Ginsenoside Rh2 and compound K induced the downregulation of the [3H]MK-801 binding as well as upregulation of the and [3H]muscimol binding in a region-specific manner after prolonged infusion into lateral ventricle. However, ginsenoside Rg3 did not show the significant changes of ligand bindings. In addition, ginsenoside Rh2 decreased the expression of nNOS in the hippocampus although Rg3 decreased the expression in the cortex. These results suggest that biotransformed ginsenoside Rh2 and compound K could play an important role in the biological activities in the central nervous systems and neurodegenerative disease.
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PMID:Changes of [3H]MK-801, [3H]muscimol and [3H]flunitrazepam binding in rat brain by the prolonged ventricular infusion of transformed ginsenosides. 1567 48

Ginseng root is one of the most popular herbs throughout the world and is believed to be a panacea and to promote longevity. It has been used as a medicine to protect against cardiac ischemia, a major cause of death in the West. We have previously demonstrated that ginsenoside Re, a main phytosterol of Panax ginseng, inhibits Ca(2+) accumulation in mitochondria during cardiac ischemia/reperfusion, which is attributable to nitric oxide (NO)-induced Ca(2+) channel inhibition and K(+) channel activation in cardiac myocytes. In this study, we provide compelling evidence that ginsenoside Re activates endothelial NO synthase (eNOS) to release NO, resulting in activation of the slowly activating delayed rectifier K(+) current. The eNOS activation occurs via a nongenomic pathway of each of androgen receptor, estrogen receptor-alpha, and progesterone receptor, in which c-Src, phosphoinositide 3-kinase, Akt, and eNOS are sequentially activated. However, ginsenoside Re does not stimulate proliferation of androgen-responsive LNCaP cells and estrogen-responsive MCF-7 cells, implying that ginsenoside Re does not activate a genomic pathway of sex hormone receptors. Fluorescence resonance energy transfer experiments with a probe, SCCoR (single cell coactivator recruitment), indicate that the lack of genomic action is attributable to failure of coactivator recruitment. Thus, ginsenoside Re acts as a specific agonist for the nongenomic pathway of sex steroid receptors, and NO released from activated eNOS underlies cardiac K(+) channel activation and protection against ischemia-reperfusion injury.
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PMID:Ginsenoside Re, a main phytosterol of Panax ginseng, activates cardiac potassium channels via a nongenomic pathway of sex hormones. 1698 85

Ginseng Radix, Atractylodis Macrocephalae Rhizoma, Poria, Glycyrrhizae Radix, Angelicae Gigantis Radix, Ligusticum Rhizoma, Rehmanniae Radix, Paeoniae Radix, Acori Graminei Rhizoma, and Polygalae Radix have been widely used as herbal medicine against ischemia. In order to test the neuroprotective effect of a novel prescription, the present study examined the effects of Palmul-Chongmyeong-Tang (PMCMT) consisting of these ten herbs on learning and memory in the Morris water maze task and the central cholinergic system of rats with cerebral ischemia-induced neuronal and cognitive impairments. After middle cerebral artery occlusion (MCAO) for 2 h, rats were administered with saline or PMCMT (200 mg/kg, p.o.) daily for 2 weeks, followed by their training to the tasks. In the water maze test, the animals were trained to find a platform in a fixed position during 6 d and then received a 60 s probe trial on the 7th day following removal of the platform from the pool. Rats with ischemic insults showed impaired learning and memory of the tasks and treatment with PMCMT produced a significant improvement in escape latency to find the platform in the Morris water maze. Consistent with behavioral data, treatment with PMCMT also reduced the loss of cholinergic immunoreactivity in the hippocampus induced by cerebral ischemia. These results demonstrated that PMCMT has a protective effect against ischemia-induced neuronal and cognitive impairments. The present study suggested that PMCMT might be useful in the treatment of vascular dementia.
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PMID:Neuroprotective effect of palmul-chongmyeong-tang on ischemia-induced learning and memory deficits in the rat. 1726 76

We previously found that ginsenoside Rd (GSRd), one of the main active ingredients in Panax Ginseng, attenuates H(2)O(2)-induced oxidative injury in PC12 cells. Mounting evidence suggests that the oxidative stress is crucially involved in the pathophysiologic process of ischemia. In the present study, we examined the protective role of GSRd to attenuate ischemic neuronal injury in vitro. Cultured hippocampal neurons were exposed to oxygen-glucose deprivation (OGD) for 2h followed by a 24-h reoxygenation. GSRd exhibited remarkable neuroprotection when presented during OGD and reoxygenation, which may be ascribed to its antioxidative properties by reducing the intracellular reactive oxygen species and malondialdehyde production; increasing glutathione content; and enhancing the antioxidant enzymatic activities of catalase, superoxide dismutase and glutathione peroxidase. Additionally, GSRd could stabilize the mitochondrial membrane potential and attenuate apoptotic death of hippocampal neurons after OGD exposure. These findings suggested that GSRd may be a potential neuroprotective agent for cerebral ischemic injury and should encourage further in vivo studies on stroke to explore the potential neuroprotective efficacy of GSRd.
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PMID:Neuroprotective effects of ginsenoside Rd against oxygen-glucose deprivation in cultured hippocampal neurons. 1944


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