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How I ‘Cured' My DepressionGinseng for depression -
Ginsenoside Rb1 also decreased the expression of TNF-α, down regulated IL-6 expression, inhibited the activation of NF-κB and modulated microglial activation after brain ischemia Zhu et al. Ginsenoside Rg1 pre-treatment of LPS induced BV-2 microglial cells activated the phospholipase C signaling pathway and modulated the expression of iNOS, COX-2, TNF-α, IL-1β and NF-κB Zong et al.
A ginseng saponin metabolite, compound K O-D-glucopyranosyl S -PD , reduced the number of Iba1-positive activated microglia, and inhibited the expression of TNF-α and IL-1β in the brain after LPS-induced sepsis Park et al.
Together, results indicate that ginseng has anti-neuroinflammatory effects by reducing activation of microglia. Moreover, total saponins in the leaves of Panax notoginseng reduced H 2 O 2 induced cell death in primary rat cortical astrocytes, likely through nuclear translocation of Nrf2 and upregulation of antioxidant systems including HO-1 and glutathione S-transferase Zhou et al.
In contrast to normal or hypoxic astrocytes, ginsenoside Rg3 showed anti-cancer activities in malignant astrocytes glioblastoma multiforme cells, by induction of apoptosis via the methyl ethyl ketone MEK signaling pathway Choi et al.
Ginsenosides may be effective in inhibiting changes to the cerebral microvasculature after cerebral ischemia. Ginsenoside Rg1 also modulated increase in aquaporin 4 expression and blood brain barrier BBB disruption after cerebral ischemia in rats Zhou et al. They are associated with progressive loss of cognitive function and motor disabilities with devastating consequences to the affected individual.
Genetic factors, environmental factors and unhealthy lifestyle have been suggested to contribute to the pathogenesis of neurodegenerative processes Farooqui, ; Seidl et al. Many neurodegenerative diseases are accompanied by oxidative stress and neuroinflammation, and associated with increased generation of lipid mediators, abnormal protein aggregation, slow excitotoxicity, loss of synapses and disintegration of neural networks, leading to failure of neurological functions Jellinger, ; Farooqui, Neurotraumatic diseases are caused by metabolic or mechanical insult to the brain and spinal cord.
They include cerebral ischemia or stroke, spinal cord injury and traumatic brain injury. Neurochemical events in neurotraumatic diseases include the release of glutamate, overstimulation of glutamate receptors, rapid calcium influx, activation of cytosolic phospholipase A 2 cPLA 2 , phospholipase C, COX-2 and NOS, induction of oxidative stress and neuroinflammation Farooqui, Neuropsychiatric disorders include both neurodevelopmental disorders and behavioral or psychological difficulties such as depression, schizophrenia, and bipolar disorders.
Impairment of cognitive processes results in behavioral symptoms such as abnormal thoughts or actions, delusions, and hallucinations. They involve abnormalities in the cerebral cortex, ventral striatum and other components of the limbic system Gallagher, AD is the most common form of dementia, a general term for memory loss and other intellectual abilities serious enough to interfere with daily life.
It is characterized by the presence of extracellular plaques consisting of aggregated Aβ peptides and neurofibrillary tangles that contains hyperphosphorylated tau protein, as well as cerebral amyloid angiopathy, due to Aβ deposition around the walls of arterioles or capillaries in the brain Reviewed in Cheng et al.
Aβ peptides are generated from amyloid precursor protein APP by β-secretase BACE1 and γ-secretase activities, and are generally considered to be toxic to neurons, while neurofibrillary tangles interfere with cellular transport processes. These flavonol glycosides also reduced memory impairment in a passive avoidance task in scopolamine-treated rats Choi et al.
Treatment of SH-SY5Y neuroblastoma cells with gintonin, a novel LPA1 receptor activating ligand decreased Aβ1—42 release, and attenuated Aβ1—40 induced toxicity. In addition, long-term oral administration of gintonin attenuated amyloid plaque deposition, and short- and long-term memory impairment in a mouse model of AD Hwang et al.
Fermented ginseng also reduced Aβ1—42 levels in HeLa cells stably expressing the Swedish mutant form of APP and decreased memory impairment in mouse models of AD Kim et al. Table 2. Studies summarizing the effects of ginseng metabolites in neurological disorders. Ginseng may have beneficial effects in AD by reducing the formation of Aβ oligomers Figure 2.
Chronic supplementation with ginsenosides for 8 months in the drinking water modulated age-related memory impairment in mice Zhao et al. Panax notoginseng saponins reduced brain APP mRNA levels and improved learning and memory in senescence-accelerated mice Zhong et al.
Ginsenosides CK, F1, Rh1 and Rh2 from Panax ginseng were found to have potential BACE1 inhibitory activities Karpagam et al. Ginsenoside Rh2 improved learning and memory performance, and reduced the number of senile plaques in brains of Tg mice Qiu et al.
Results suggest neuroprotective effects of ginsenosides by reducing Aβ levels via stimulation of α-secretase activity and inhibition of β-secretase activity. Ginseng may also have a beneficial effect in AD by reducing tau hyperphosphorylation and neurofibrillary tangle formation.
Total ginsenoside extracts from stems and leaves of Panax ginseng enhanced the phosphatase activity of purified calcineurin. This could be useful in AD, since inhibition of calcineurin leads to tau hyperphosphorylation at multiple sites in AD brains Tu et al.
Ginsenoside Rb1 reversed aluminum exposure-induced decreased PP2A level and tau phosphorylation in the cortex and hippocampus Zhao et al. Results suggest neuroprotective effect of ginsenosides by reducing tau hyperphosphorylation.
Ginsenosides are reported to have antioxidant effects. Rg1 is a potential regulator of hypoxia-inducible factor-1α HIF-1α , and could act via this transcription factor to improve cell survival, angiogenesis and neurogenesis Tang et al.
Oral treatment with pseudoginsenoside-F11 PF11 , a component of Panax quinquefolium increased the activity of antioxidant enzymes superoxide dismutase SOD and glutathione peroxidase GSH-Px , and is associated with improved learning and memory in a mouse model of AD Wang et al.
Ginsenoside Rg1 treatment modulated Aβ 25—35 induced mitochondrial dysfunction, inhibition of HIF-1α expression and increase in reactive nitrogen species and protein nitrotyrosination in human endothelial cells Yan et al. Loss of ACh is found in the brain in AD.
Ginsenoside Rg5 found in Panax ginseng modulated cognitive dysfunction and neuroinflammation in the brains of streptozotocin-induced memory impaired rats. Acetylcholinesterase AChE activity was reduced, while choline acetyltransferase ChAT activity was increased in the cortex of Rg5 treated rats Chu et al.
In the long-term evaluation of the efficacy of Korean Red Ginseng in patients after 24 weeks, the Korean version of the Mini Mental Status Examination K-MMSE score remained without significant decline at the 48 th and 96 th weeks, and similar results were obtained with ADAS.
Together, results point to long-term beneficial effects of Korean Red Ginseng in patients with AD Heo et al. Major depressive disorder or major depression is a mental disorder characterized by a pervasive and persistent low mood that is accompanied by low self-esteem and by a loss of interest or pleasure in normally enjoyable activities.
They also reversed the reduction in the sucrose preference index, decrease in locomotor activity, as well as prolongation of latency of feeding in a novel environment, in a chronic stress model of depression in rats Dang et al.
Ginseng saponins also had antidepressant effects in the corticosterone-induced mouse model of depression Chen et al. Levels of 5-hydroxytryptamine, dopamine, and noradrenaline were increased in the brains of treated rats, which could be the basis of the antidepressant effects Xiang et al.
Ginsenoside Rg1 upregulated BDNF signaling in the hippocampus, down regulated serum corticosterone levels, and reversed the decrease in dendritic spine density and hippocampal neurogenesis caused by chronic stress Jiang et al. A post-metabolism compound and intestinal metabolite of ingested ginsenosides, PD, showed antidepressant effects in the tail suspension and forced swim tests, in the olfactory bulbectomy rat model of depression Xu et al.
A randomized, multicenter, double-blind parallel group study of post-menopausal women treated with ginseng and treated with placebo reported significant difference in depression scores in favor of ginseng compared with placebo Wiklund et al.
Another study of possible casual relation between hormones, energy sources, and minerals indicated that depression was related to serum lipids including cholesterol, and that fermented red ginseng had beneficial effects on depression by modulating this relation Lee and Ji, Stroke or cerebrovascular event is associated with a sudden loss of brain function, due to disturbance in blood supply to the brain.
Interestingly, ginsenoside Rd demonstrated neuroprotection even when administered 4 h after recirculation of transient MCAO or after onset of ischemic stroke induced by permanent MCAO Ye et al.
High dose ginsenoside Rb1 treatment reduced neurological deficits, brain edema, BBB disruption and the number of terminal deoxynucleotidyl transferase dUTP nick end labeling TUNEL positive cells after hemorrhagic stroke Li et al.
Significant reduction in basilar artery vasospasm and lumen thickness was also observed after Rb treatment Li et al. Results suggest that neuroprotective effect of ginseng in stroke via inhibition of ion channels or modulation of vasospasm. It is, however, noted that ginseng may have a drug interaction with the anticoagulant warfarin that could lead to increased risk of bleeding, and this should be taken into consideration in patients who are on warfarin.
Parkinson disease is a neurodegenerative disorder affecting mainly the motor system, as a result of death of dopaminergic neurons in the substantia nigra. These compounds exert neuroprotective effects through inhibition of oxidative stress and neuroinflammation, decrease in toxin-induced apoptosis and nigral iron levels, and regulation of N-methyl-D-aspartate receptor channel activity reviewed by González-Burgos et al.
MPTP administration resulted in behavioral impairment, dopaminergic neuronal death, and increased Cdk5 and p25 expression but decreased p35 expression in the nigrostriatal system of mice, and these effects were modulated by Korean Red Ginseng Jun et al.
Panaxatriol saponins, the main constituents extracted from Panax notoginseng provided neuroprotection against loss of dopaminergic neurons and behavioral impairment after MPTP treatment Luo et al.
Ginsenoside Rd has been studied in an animal model of multiple sclerosis, EAE. Many ginsenosides have been isolated and characterized. The molecular mechanisms associated with ginsenosides involve scavenging free radicals, inhibition of inflammation, and prevention of excitotoxicity.
Animal and cell culture studies have indicated that ginsenosides have different activities in both physiological and pathologic conditions. The structure activity relationship of ginsenosides has not been fully elucidated.
However, it is becoming increasingly evident that ginsenosides produce neuroprotective effects by reducing free radical production and enhancing brain function. Studies involving each ginsenoside should include mechanisms of action, specificity, structure and function relationship, detailed pharmacokinetics and toxicity studies, and therapeutic studies in animal models and humans.
The neurological disorders for which there is most evidence from pre-clinical and a small number of clinical studies to benefit from ginseng are AD and major depression, and clinical trials are necessary to confirm the efficacy of ginseng and ginsenosides in the prevention and treatment of these, and possibly other neurological conditions.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
This work was supported by grants from the National University Health System and the National Medical Research Council of Singapore. Attele, A. Ginseng pharmacology: multiple constituents and multiple actions. doi: PubMed Abstract CrossRef Full Text Google Scholar.
Bae, E. Planta Med. Baek, S. Recent methodology in ginseng analysis. Ginseng Res. Bowie, L. Effects of an aqueous extract of North American ginseng on MOG -induced EAE in mice.
Chang, Y. Panax ginseng: a role in cancer therapy? Cancer Ther. Chen, R. Acta Pharmacol. Chen, Z. Neuroprotective effect of ginsenoside Rb1 on glutamate-induced neurotoxicity: with emphasis on autophagy. Chen, G. Comparative analysis on microbial and rat metabolism of ginsenoside Rb1 by high-performance liquid chromatography coupled with tandem mass spectrometry.
Microbial transformation of ginsenoside Rb 1 by Acremonium strictum. Chen, L. PubMed Abstract Google Scholar. Cheng, Y. Anti-amnestic and anti-aging effects of ginsenoside Rg1 and Rb1 and its mechanism of action.
Choi, S. Structure of ginseng major latex-like protein and its proposed lysophosphatidic acid-binding mechanism. Acta Crystallogr. D Biol. Choi, K. Ginsenosides compound K and Rh 2 inhibit tumor necrosis factor-alpha-induced activation of the NF-kappaB and JNK pathways in human astroglial cells.
Choi, Y. Ginsenoside Rg3 induces apoptosis in the U87MG human glioblastoma cell line through the MEK signaling pathway and reactive oxygen species. Choi, R. Alzheimers Dis. Choo, M. Antiallergic activity of ginseng and its ginsenosides.
Chu, S. Ginsenoside Rg5 improves cognitive dysfunction and beta-amyloid deposition in STZ-induced memory impaired rats via attenuating neuroinflammatory responses. Cui, J. Ginsenoside Rb3 exerts antidepressant-like effects in several animal models. Dancey, J. Molecular targeting: PI3 kinase pathway.
Dang, H. Antidepressant effects of ginseng total saponins in the forced swimming test and chronic mild stress models of depression. Psychiatry 33, — A double-blind, placebo-controlled clinical study on the effect of a standardized ginseng extract on psychomotor performance in healthy volunteers.
Du, X. Fang, F. Multi-faced neuroprotective effects of Ginsenoside Rg1 in an Alzheimer mouse model. Acta , — Farooqui, A.
Neurochemical Aspects of Neurotraumatic and Neurodegenerative Diseases. New York: Springer. Google Scholar.
Fu, Y. Chronic ginseng consumption attenuates age-associated oxidative stress in rats. Fuzzati, N. Analysis methods of ginsenosides. B Analyt. Life Sci. Gallagher, S.
Neurocognitive models of schizophrenia: a neurophenomenological critique. Psychopathology 37, 8— Gao, Y. González-Burgos, E. PubMed Abstract CrossRef Full Text. Hao, K. Beneficial estrogen-like effects of ginsenoside Rb1, an active component of Panax ginseng, on neural 5-HT disposition and behavioral tasks in ovariectomized mice.
Hasegawa, H. Proof of the mysterious efficacy of ginseng: basic and clinical trials: metabolic activation of ginsenoside: deglycosylation by intestinal bacteria and esterification with fatty acid.
Role of human intestinal Prevotella oris in hydrolyzing ginseng saponins. Antimetastatic efficacy of orally administered ginsenoside Rb1 in dependence on intestinal bacterial hydrolyzing potential and significance of treatment with an active bacterial metabolite.
He, B. Neuroprotective effect of 20 R -ginsenoside Rg 3 against transient focal cerebral ischemia in rats. He, Q. Neuroprotective effects of ginsenoside Rg1 against oxygen-glucose deprivation in cultured hippocampal neurons.
Heo, J. Hou, J. Highly selective microbial transformation of major ginsenoside Rb1 to gypenoside LXXV by Esteya vermicola CNU Hsieh, W. Food Chem. Huang, J. Effects of Panax notoginseng saponin on alpha, beta and gamma secretase involved in Abeta deposition in SAMP8 mice.
Neuroreport 25, 89— Hwang, S. Gintonin, a novel ginseng-derived lysophosphatidic acid receptor ligand, stimulates neurotransmitter release. Gintonin, newly identified compounds from ginseng, is novel lysophosphatidic acids-protein complexes and activates G protein-coupled lysophosphatidic acid receptors with high affinity.
Cells 33, — Itoh, T. Effects of Panax ginseng root on the vertical and horizontal motor activities and on brain monoamine-related substances in mice. Jang, S. Changes of [3H]MK, [3H]muscimol and [3H]flunitrazepam binding in rat brain by the prolonged ventricular infusion of transformed ginsenosides.
Jellinger, K. Recent advances in our understanding of neurodegeneration. Neural Transm. Jeong, H. Effect of Korean Red Ginseng as an adjuvant treatment for women with residual symptoms of major depression.
Asia Pac. Psychiatry doi: Jia, D. Neuroprotective effect of Panax notoginseng plysaccharides against focal cerebral ischemia reperfusion injury in rats.
Jiang, Y. Zhongguo Zhong Yao Za Zhi 37, — Jiang, B. Antidepressant-like effects of ginsenoside Rg1 are due to activation of the BDNF signalling pathway and neurogenesis in the hippocampus. Jun, Y. Jung, I. Metabolism of ginsenoside Rb1 by human intestinal microflora and cloning of its metabolizing beta-D-glucosidase from Bifidobacterium longum H Jung, J.
Anti-inflammatory mechanism of ginsenoside Rh1 in lipopolysaccharide-stimulated microglia: critical role of the protein kinase A pathway and hemeoxygenase-1 expression. Karpagam, V. Identification of BACE1 inhibitors from Panax ginseng saponins-An Insilco approach.
Keum, Y. Inhibitory effects of the ginsenoside Rg3 on phorbol ester-induced cyclooxygenase-2 expression, NF-kappaB activation and tumor promotion. Kiefer, D. Panax ginseng. Physician 68, — Kim, S. Inhibitory effect of ginsenosides on NMDA receptor-mediated signals in rat hippocampal neurons.
Kim, J. Kim, E. Anti-oxidative stress effect of red ginseng in the brain is mediated by peptidyl arginine deiminase type IV PADI4 repression via estrogen receptor ER beta up-regulation. Kim, Y. Kim, M. Ginsenoside Re and Rd enhance the expression of cholinergic markers and neuronal differentiation in Neuro-2a cells.
Lee, Y. Ginsenoside-Rg1, one of the major active molecules from Panax ginseng, is a functional ligand of glucocorticoid receptor. Lee, K. The effect of fermented red ginseng on depression is mediated by lipids. Lee, J.
Adaptive cellular stress pathways as therapeutic targets of dietary phytochemicals: focus on the nervous system. Effects of ginsenoside Re on LPS-induced inflammatory mediators in BV2 microglial cells. BMC Complement. Lee, S. Proteomic analysis of the anti-cancer effect of 20S-ginsenoside Rg3 in human colon cancer cell lines.
Leung, K. Signaling pathway of ginsenoside-Rg1 leading to nitric oxide production in endothelial cells. FEBS Lett. Li, M. Zhong Xi Yi Jie He Xue Bao 4, — Li, L. Protective effects of ginsenoside Rd against okadaic acid-induced neurotoxicity in vivo and in vitro. Li, Y.
Treatment with ginsenoside rb1, a component of panax ginseng, provides neuroprotection in rats subjected to subarachnoid hemorrhage-induced brain injury.
Acta Neurochir. Ginsenoside Rbeta1 reduces neurologic damage, is anti-apoptotic and down-regulates p53 and BAX in subarachnoid hemorrhage. Zhongguo Zhong Yao Za Zhi 38, — Lin, Z.
Ginsenoside Rb1 selectively inhibits the activity of L-type voltage-gated calcium channels in cultured rat hippocampal neurons. Lin, T. Promotive effect of ginsenoside Rd on proliferation of neural stem cells in vivo and in vitro. Liu, L. Ginsenoside Rb1 improves spatial learning and memory by regulation of cell genesis in the hippocampal subregions of rats.
Brain Res. They are strongly supported as effective by scientific evidence. These treatments are useful. They are supported by scientific evidence as effective, but the evidence is not as strong.
These treatments are promising and may be useful. They have some evidence to support them, but more evidence is needed to be sure they work. On the available evidence, these treatments do not seem to be effective.
These treatments have not been properly researched. It is not possible to say whether they are useful or not. Safety or other concerns have been raised for the use of these treatments.
What is it? How does it work? Is it effective? Are there any disadvantages? Where do you get it? Recommendation There is not enough good evidence at this stage to recommend ginseng as a treatment for depression.
Key references Geller SE, Studee L. Botanical and dietary supplements for mood and anxiety in menopausal women. Menopause New York, NY. Kennedy DO, Scholey AB. Ginseng: potential for the enhancement of cognitive performance and mood. Pharmacology, biochemistry, and behavior. Lee KJ, Ji GE.
The effect of fermented red ginseng on depression is mediated by lipids.
Overview of ginseng as a natural remedy for depression Ginsfng whether Ginseng for depression works Ginseng for depression Boost cognitive function depression. The roots of Ginseng for depression ginseng plant Ginseg used as a medicine, particularly in Oriental countries. There are three types of ginseng plant: Chinese ginseng Latin name: Panax ginsengAmerican ginseng Panax quinquefolius and Siberian ginseng Eleutherococcus senticosus. Chinese and American ginseng are closely related plant species, while Siberian ginseng is a more distantly related plant. All are thought to have similar medicinal effects. Others will tell you it can do everything from improving brain depreseion to regulating depresssion sugar. Meal planning for specific diets species of deprssion have been used for thousands of Ginseng for depression across different Ginseng for depression and cultures. Find out why Ginseng for depression is an essential nutrient ». Some claim that it can reduce stress, alleviate erectile dysfunction, ward off dementia, strengthen the immune system, prevent cold or flu, reduce infections, improve digestion, and even cure cancer. One of the main reasons people take ginseng is because of its antioxidant properties. Antioxidants, which are molecules that inhibit the oxidation of other molecules, are very much in vogue right now. Since oxidation can cause the growth of free radicals, a lot of research Gonseng gone into determining if antioxidants can actually fight cancer.
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