人蔘(人參)的營養成份及藥用功效: health care with eating ginseng.

Panax ginseng is especially prized throughout the worl energy, virility and mental clarity.

Dr. Andrew Weil, a world famous medical doctor who advocates the use of integrative approaches to healthyd for its role in promoting healthy aging, sexual aging, also includes Panax ginseng in his recommendations for sexual potency. He describes Panax ginseng as “a good stimulant and sexual energizer” that boosts energy overall and helps dispel occasional fatigue.

"These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat cure, or prevent and disease."

Ginseng, the root of Panax species, is a well-known herbal medicine. It has been used as a traditional medicine in China, Korea, and Japan for thousands of years and is now a popular and worldwide used natural medicine.

The active ingredients of ginseng are ginsenosides which are also called ginseng saponins. Recently, there is increasing evidence in the literature on the pharmacological and physiological actions of ginseng.However, ginseng has been used primarily as a tonic to invigorate weak bodies and help the restoration of homeostasis. Current in vivo and in vitro studies have shown its beneficial effects in a wide range of pathological conditions such as cardiovascular diseases, cancer, immune deficiency, and hepatotoxicity. Moreover, recent research has suggested that some of ginseng's active ingredients also exert beneficial effects on aging, central nervous system (CNS) disorders, and neurodegenerative diseases. In general, antioxidant, anti-inflammatory, anti-apoptotic, and immune-stimulatory activities are mostly underlying the possible ginseng-mediated protective mechanisms. Next to animal studies, data from neural cell cultures contribute to the understanding of these mechanisms that involve decreasing nitric oxide (NO), scavenging of free radicals, and counteracting excitotoxicity.

In this review, we focus on recently reported medicinal effects of ginseng and summarize the current knowledge of its effects on CNS disorders and neurodegenerative diseases.

Neural progenitor cells (NPCs) exist not only in the developing brain, but also in certain areas in adult brain in mammals.

Recent studies suggest that promoting neurogenesis in adult mammals might provide a therapeutic way to cure age-related neurodegenerative diseases. So, it will be of great value to find out drugs that can increase the proliferation and/or differentiation ability of neural progenitors. The present study investigated the influence of ginsenoside Rg1, an active ingredient of Panax ginseng C.A. Meyer, on proliferation ability of rodent hippocampal progenitor cells both in vitro and in vivo. Incubation of NPCs with ginsenoside Rg1 resulted in significant increase in absorbency value, 3H-thymidine incorporation and the number of proliferating progenitor cell spheres; In addition, 2 weeks Rg1 administration (i.p.) led to marked enhancement of the number of dividing cells in the hippocampus of adult mice.

These findings suggest that ginsenoside Rg1 is involved in the regulation of proliferation of hippocampal progenitor cells and this effect may serve as one of the elementary mechanisms underlying its nootropic and anti-aging actions.

Copyright 2004 W.S. Maney and Son Ltd

In Chinese medicine, ginseng (Panax ginseng C.A. Meyer) has long been used as a general tonic or an adaptogen to promote longevity and enhance bodily functions. It has also been claimed to be effective in combating stress, fatigue, oxidants, cancer and diabetes mellitus. Most of the pharmacological actions of ginseng are attributed to one type of its constituents, namely the ginsenosides.

In this review, we focus on the recent advances in the study of ginsenosides on angiogenesis which is related to many pathological conditions including tumor progression and cardiovascular dysfunctions. Angiogenesis in the human body is regulated by two sets of counteracting factors, angiogenic stimulators and inhibitors. The 'Yin and Yang' action of ginseng on angiomodulation was paralleled by the experimental data showing angiogenesis was indeed related to the compositional ratio between ginsenosides Rg1 and Rb1. Rg1 was later found to stimulate angiogenesis through augmenting the production of nitric oxide (NO) and vascular endothelial growth factor (VEGF). Mechanistic studies revealed that such responses were mediated through the PI3K-->Akt pathway. By means of DNA microarray, a group of genes related to cell adhesion, migration and cytoskeleton were found to be up-regulated in endothelial cells. These gene products may interact in a hierarchical cascade pattern to modulate cell architectural dynamics which is concomitant to the observed phenomena in angiogenesis. By contrast, the anti-tumor and anti-angiogenic effects of ginsenosides (e.g. Rg3 and Rh2) have been demonstrated in various models of tumor and endothelial cells, indicating that ginsenosides with opposing activities are present in ginseng.

Ginsenosides and Panax ginseng extracts have been shown to exert protective effects on vascular dysfunctions, such as hypertension, atherosclerotic disorders and ischemic injury. Recent work has demonstrates the target molecules of ginsenosides to be a group of nuclear steroid hormone receptors. These lines of evidence support that the interaction between ginsenosides and various nuclear steroid hormone receptors may explain the diverse pharmacological activities of ginseng. These findings may also lead to development of more efficacious ginseng-derived therapeutics for angiogenesis-related diseases.

Skin aging appears to be principally related to a decrease in levels of Type I collagen, the primary component of the dermal layer of skin. It is important to introduce an efficient agent for effective management of skin aging; this agent should have the fewest possible side effects and the greatest wrinkle-reducing effect.

In the course of screening collagen production-promoting agents, we obtained Panax ginseng C.A. Meyer. This study was designed to investigate the possible collagen production-promoting activities of Panax ginseng C.A. Meyer root extract (PGRE) in human dermal fibroblast cells. As a first step to this end, human COL1A2 promoter luciferase assay was performed in human dermal fibroblast cells. In this assay, PGRE activated human COL1A2 promoter activity in a concentration-dependent manner. Human Type I procollagen synthesis was also induced by PGRE. These results suggest that PGRE promotes collagen production in human dermal fibroblast cells. Additionally, we have attempted to characterize the mechanism of action of PGRE in Type I procollagen synthesis. PGRE was found to induce the phosphorylation of Smad2, an important transcription factor in the production of Type I procollagen. When applied topically in a human skin primary irritation test, PGRE did not induce any adverse reactions.

Therefore, based on these results, we suggest the possibility that PGRE may be considered as an attractive, wrinkle-reducing candidate for topical application.

Ginseng, the root of the Panax species, is a well-known herbal medicine.

Traditionally it has been used in Korea, China and Japan for thousands of years. Nowadays it has become a popular and worldwide known health drug. Current scientific studies demonstrate in vivo and in vitro its beneficial effects in a wide range of pathological conditions such as cardiovascular disease, cancer, immune deficiency and hepatotoxicity. Ginsenosides or ginseng saponins as the active ingredients have antioxidant, anti-inflammatory, anti-apoptotic and immunostimulant properties, which raised speculations that these compounds could positively affect neurodegenerative disorders and delay neuronal aging. Conclusive clinical data in humans are still missing.

However, results from animal studies and neuronal cell culture experiments indicate that ginsenosides can counteract and attenuate factors promoting neuronal death as environmental toxins, excitotoxic action of glutamate and rises in intracellular calcium, excessive release of free radicals and apoptotic events.

Thus, neuroprotective actions of ginsenosides could come about as a valuable option to slow down neurodegenerative diseases.

Ginseng, the root of Panax ginseng C.A. Meyer (Araliaceae), has been extensively used in traditional oriental medicine for the prevention and treatment of aging-related disorders for over 2000 years. Accumulating evidence suggests that ginsenosides such as Rg1 and Rb1, which are the pharmacologically active ingredients of ginseng, modulate neurotransmission. Synapsins are abundant phosphoproteins essential for regulating neurotransmitter release. All synapsins contain a short amino-terminal domain A that is highly conserved and phosphorylated by cAMP-dependent protein kinase (PKA), which plays a key role in regulating neurotransmitter release.

In the present study, we demonstrated that both Rg1 and Rb1 increased neurotransmitter release in undifferentiated and differentiated PC12 cells. However, in the presence of the PKA inhibitor H89, Rg1, but not Rb1, still induced neurotransmitter release. Moreover, Rb1, but not Rg1, enhanced the phosphorylation of synapsins via PKA pathway.

In summary, Rb1 promotes neurotransmitter release by increasing the phosphorylation of synapsins through the PKA pathway, whereas the similar effects observed with Rg1 are independent of the phosphorylation of synapsins.

In the present paper, we overview the discovery of new biological activities induced by ginsenoside Rg1 and Rb1 and discuss possible mechanisms of action. Both compounds could increase neural plasticity in efficacy and structure; especially Rg1, as one small molecular drug, can increase proliferation and differentiation of neural progenitor cells in dentate gyrus of hippocampus of normal adult mice and global ischemia model in gerbils.

This finding has great value for treatment of Alzheimer's disease and other neurodegenerative disorders which is characterized by neurons loss. Increase of expression of brain derived neurotrophic factor, Bcl-2 and antioxidant enzyme, enhanced new synapse formation, inhibition of apoptosis and calcium overload are also important neuron protective factors. Rg1 and Rb1 have common effects, but there are some differences in pharmacology and mechanism.

These differences may attribute to their different chemical structure. Rg1 is panaxtriol with two sugars, while Rb1 is panaxtriol with four sugars.

Most of the known pharmacological effects of Panax ginseng on the central nervous system are due to its major components - ginsenosides.

Although the antioxidant ability of ginseng root has already been established, this activity has never been evaluated for isolated ginsenosides on astrocytes. The activity of protopanaxadiols Rb(1), Rb(2), Rc and Rd, and protopanaxatriols Re and Rg(1) was evaluated in vitro on astrocytes primary culture by means of an oxidative stress model with H(2)O(2). The viability of astrocytes was determined by the MTT reduction assay and by the LDH release into the incubation medium.

The effects on the antioxidant enzymes catalase, superoxide dismutase (SOD), glutathione peroxidases (GPx) and glutathione reductase (GR) and on the intracellular reactive oxygen species (ROS) formation were also investigated. Exposure of astrocytes to H(2)O(2) decreased cell viability as well as the antioxidant enzymes activity and increased ROS formation. Oxidative stress produced significant cell death that was reduced by previous treatment with the tested ginsenosides.

Ginsenosides Rb(1), Rb(2), Re and Rg(1) were effective in reducing astrocytic death, while Rb(1), Rb(2), Rd, Re and Rg(1) decreased ROS formation, ginsenoside Re being the most active. Ginsenosides from P. ginseng induce neuroprotection mainly through activation of antioxidant enzymes.

Ginsenosides, the main component of Panax ginseng, have been known for the anti-inflammatory and anti-proliferative activities. In this study, we investigated the molecular mechanisms responsible for the anti-inflammatory effects of ginsenosides on activated astroglial cells. Among 13 different ginsenosides, intestinal bacterial metabolites Rh(2) and compound K (C-K) showed a significant inhibitory effect on tumor necrosis factor-alpha (TNF-alpha)-induced expression of intercellular adhesion molecule-1 in human astroglial cells. Pretreatment with C-K or Rh(2) suppressed TNF-alpha-induced phosphorylation of IkappaBalpha kinase and the subsequent phosphorylation and degradation of IkappaBalpha. Additionally, the same treatment inhibited TNF-alpha-induced phosphorylation of MKK4 and the subsequent activation of the JNK-AP-1 pathway. The inhibitory effect of ginsenosides on TNF-alpha-induced activation of the NF-kappaB and JNK pathways was not observed in human monocytic U937 cells.

These results collectively indicate that ginsenoside metabolites C-K and Rh(2) exert anti-inflammatory effects by the inhibition of both NF-kappaB and JNK pathways in a cell-specific manner.

Ginseng, the root of Panax ginseng, has been used as folk medicine in the treatment of various diseases for thousands of years in China. Ginsenoside Rb1 (Rb1), one of the effective components of ginseng, has been reported to release nitric oxide and decrease intracellular free Ca2+ in cardiac myocytes, both of which play important roles in antihypertrophic effect. This study was to investigate the potential effect of Rb1 on right ventricular hypertrophy (RVH) induced by monocrotaline (MCT) and its possible influence on calcineurin (CaN) signal transduction pathway. MCT-treated animals were administered with Rb1 (10 and 40 mg /kg) from day 1 to day 14 (preventive administration) or from day 15 to day 28 (therapeutic administration), or with vehicle as corresponding controls. After 2 weeks, significantly hypertrophic reactions, including RVH index and the expressions of atrial natriuretic peptide mRNA, appeared in right ventricle of all MCT-treated animals (p <>

These results suggest that Rb1 treatment can inhibit the RVH induced by MCT, which may be involved in its inhibitory effects on CaN signal transduction pathway.

Ginsenoside Rb1 (Rb1), ginsenoside Rg1 (Rg1), and notoginsenoside R1 (R1) are major active components of Panax notoginseng, a Chinese herb that is widely used in traditional Chinese medicine to enhance blood circulation and dissipate blood stasis. To evaluate the effect of these saponins on microcirculatory disturbance induced by lipopolysaccharide (LPS), vascular hemodynamics in rat mesentery was observed continuously during their administration using an inverted microscope and a high speed video camera system. LPS administration decreased red blood cell velocity but Rb1, Rg1, and R1 attenuated this effect. LPS administration caused leukocyte adhesion to the venular wall, mast cell degranulation, and the release of cytokines. Rb1, Rg1, and R1 reduced the number of adherent leukocytes, and inhibited mast cell degranulation and cytokine elevation. In vitro experiments using flow cytometry further demonstrated that a) the LPS-enhanced expression of CD11b/CD18 by neutrophils was significantly depressed by Rb1 and R1, and b) hydrogen peroxide (H(2)O(2)) release from neutrophils in response to LPS stimulation was inhibited by treatment with Rg1 and R1.

These results suggest that the protective effect of Rb1 and R1 against leukocyte adhesion elicited by LPS may be associated with their suppressive action on the expression of CD11b/CD18 by neutrophils. The protective effect against mast cell degranulation by Rb1 and R1, and the blunting of H(2)O(2) release from neutrophils by Rg1 and R1 suggest mechanistic diversity in the effects of Panax notoginseng saponins in the attenuation of microcirculatory disturbance induced by LPS.

Ginsenoside Rh2, one of the ginsenosides contained in the Panax ginseng root, was employed to screen the effect on insulin resistance of rats induced by a diet containing 60% fructose. Single intravenous injection of ginsenoside Rh2 decreased the plasma glucose concentrations in 60 minutes in a dose-dependent manner from 0.1 mg/kg to 1 mg/kg in rats with insulin resistance induced by fructose-rich chow. Repeated intravenous injection of ginsenoside Rh2 (1 mg/kg per injection, 3 times daily) into rats which received fructose-rich chow for 3 consecutive days decreased the value of glucose-insulin index, the product of the areas under the curve of glucose and insulin during the intraperitoneal (i.p.) glucose tolerance test. This means that ginsenoside Rh2 has an ability to improve insulin action on glucose disposal. The plasma glucose lowering action of tolbutamide, induced by the secretion of endogenous insulin, is widely used to characterize the formation of insulin resistance. Time for the loss of plasma glucose lowering response to tolbutamide (10 mg/kg, i.p.) in rats during insulin resistance induction by fructose-rich chow was also markedly delayed by the repeated treatment of ginsenoside Rh2, as compared to the vehicle-treated control.

Thus, the repeated treatment of ginsenoside Rh2 delayed the development of insulin resistance in high fructose feeding rats. Increase of insulin sensitivity by ginsenoside Rh2 was further identified using the plasma glucose lowering action of exogenous insulin in streptozotocin-induced diabetic rats (STZ-diabetic rats). Repeated injection of ginsenoside Rh2 at the same dosing (1 mg/kg, 3 times daily) into STZ-diabetic rats for 10 days made an increase of the responses to exogenous insulin. Taken together, it can be concluded that ginsenoside Rh2 has an ability to improve insulin sensitivity and it seems suitable to use ginsenoside Rh2 as an adjuvant for diabetic patients and/or the subjects wishing to increase insulin sensitivity.

Recent studies have shown that Panax ginseng has a variety of beneficial effects on the cardiovascular systems. Homocysteine (Hcy), which is derived from L-methionine (Met), has been closely associated with the increased risk of cardiovascular diseases.

In the present study, we examined whether in vivo long-term administration of ginseng saponins (GS), active ingredients of Panax ginseng, attenuate adverse vascular effects associated with chronic Met-induced hyperhomocysteinemia (H-Hcy). We found that plasma Hcy level, which was measured after 30 and 60 d, in GS (100 mg/kg)+Met co-administration group was significantly reduced when it was compared with Met alone treatment group. We could also observe the alleviation of endothelial damages of aortic artery vessels in GS (100 mg/kg)+Met co-administration group compared with Met alone treatment group. We compared aortic vasocontractile and vasodilatory responses between Met alone and GS (100 mg/kg)+Met co-treatment groups. We found that norepinephrine-induced vasocontractile responses were greatly decreased in GS (100 mg/kg)+Met co-treatment group and that carbachol-induced dilatory responses were greatly enhanced in GS (100 mg/kg)+Met co-administration groups as compared with Met alone treatment group.

The present results indicate that in vivo long-term administration of GS attenuates adverse vascular effects associated with chronic Met-induced H-Hcy in rats.

Ionizing radiations produce deleterious effects in the living organisms and the rapid technological advancement has increased human exposure to ionizing radiations enormously. There is a need to protect humans against such effects of ionizing radiation. Attempts to protect against the deleterious effects of ionizing radiations by pharmacological intervention were made as early as 1949 and efforts are continued to search radioprotectors, which may be of great help for human application. This review mainly dwells on the radioprotective potential of plant and herbal extracts.

The results obtained from in vitro and in vivo studies indicate that several botanicals such as Gingko biloba, Centella asiatica, Hippophae rhamnoides, Ocimum sanctum, Panax ginseng, Podophyllum hexandrum, Amaranthus paniculatus, Emblica officinalis, Phyllanthus amarus, Piper longum, Tinospora cordifoila, Mentha arvensis, Mentha piperita, Syzygium cumini, Zingiber officinale, Ageratum conyzoides, Aegle marmelos and Aphanamixis polystachya protect against radiation-induced lethality, lipid peroxidation and DNA damage. The fractionation-guided evaluation may help to develop new radioprotectors of desired activities.