Gintonin absorption in intestinal model systems

Lee, Byung-Hwan; Choi, Sun-Hye; Kim, Hyeonjoong; Park, Sang-Deuk; Rhim, Hyewhon; Kim, Hyoung‐Chun; Hwang, Sung‐Hee; Nah, Seung-Yeol

doi:10.1016/j.jgr.2016.12.007

Cited by 18 publications

(14 citation statements)

References 28 publications

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“…Second, gintonin also restored the hypoxia-induced damages to cell viability by increasing the release of VEGF; however, the gintonin-induced VEGF release and cell proliferation under hypoxia was attenuated by a VEGF antagonist, showing that the regulation of VEGF by gintonin might be crucial for recovering from hypoxic insults. In our previous studies, we also showed that gintonin increases the formation of VEGF in the endothelial cells of human umbilical vein [25]. Thus, combining the results of the present and previous studies, the fact that gintonin regulates the release and expression of VEGF in neural and nonneuronal cells is further substantiated.…”

Section: Discussionsupporting

confidence: 87%

Gintonin-mediated release of astrocytic vascular endothelial growth factor protects cortical astrocytes from hypoxia-induced cell damages

Choi

Kim

Cho

et al. 2019

Journal of Ginseng Research

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Background Gintonin is a ginseng-derived exogenous ligand of the G protein-coupled lysophosphatidic acid (LPA) receptor. We previously reported that gintonin stimulates gliotransmitter release in primary cortical astrocytes. Astrocytes play key roles in the functions of neurovascular systems. Although vascular endothelial growth factor (VEGF) is known to influence the normal growth and maintenance of cranial blood vessels and the nervous system, there is little information about the effect of gintonin on VEGF regulation in primary astrocytes, under normal and hypoxic conditions. Methods Using primary cortical astrocytes of mice, the effects of gintonin on the release, expression, and distribution of VEGF were examined. We further investigated whether the gintonin-mediated VEGF release protects astrocytes from hypoxia. Results Gintonin administration stimulated the release and expression of VEGF from astrocytes in a concentration- and time-dependent manner. The gintonin-mediated increase in the release of VEGF was inhibited by the LPA1/3 receptor antagonist, Ki16425; phospholipase C inhibitor, U73122; inositol 1,4,5-triphosphate receptor antagonist, 2-APB; and intracellular Ca 2+ chelator, BAPTA. Hypoxia further stimulated astrocytic VEGF release. Gintonin treatment stimulated additional VEGF release and restored cell viability that had decreased due to hypoxia, via the VEGF receptor pathway. Altogether, the regulation of VEGF release and expression and astrocytic protection mediated by gintonin under hypoxia are achieved via the LPA receptor–VEGF signaling pathways. Conclusion The present study shows that the gintonin-mediated regulation of VEGF in cortical astrocytes might be neuroprotective against hypoxic insults and could explain the molecular basis of the beneficial effects of ginseng on the central nervous system.

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Section: Discussionsupporting

confidence: 87%

Gintonin-mediated release of astrocytic vascular endothelial growth factor protects cortical astrocytes from hypoxia-induced cell damages

Choi

Kim

Cho

et al. 2019

Journal of Ginseng Research

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“…Orally administered medicines are normally absorbed by the gastrointestinal layer. Lee et al showed that gintonin is significantly absorbed by the intestine [ 14 ].…”

Section: Absorption Of Gintoninmentioning

confidence: 99%

Ongoing Research on the Role of Gintonin in the Management of Neurodegenerative Disorders

Ikram

Ullah

Khan

et al. 2020

Cells

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Neurodegenerative disorders, namely Parkinson’s disease (PD), Huntington’s disease (HD), Alzheimer’s disease (AD), and multiple sclerosis (MS), are increasingly major health concerns due to the increasingly aged population worldwide. These conditions often share the same underlying pathological mechanisms, including elevated oxidative stress, neuroinflammation, and the aggregation of proteins. Several studies have highlighted the potential to diminish the clinical outcomes of these disorders via the administration of herbal compounds, among which gintonin, a derivative of ginseng, has shown promising results. Gintonin is a noncarbohydrate/saponin that has been characterized as a lysophosphatidic acid receptor (LPA Receptor) ligand. Gintonin may cause a significant elevation in calcium levels [Ca2+]i intracellularly, which promotes calcium-mediated cellular effects via the modulation of ion channels and cell surface receptors, regulating the inflammatory effects. Years of research have suggested that gintonin has antioxidant and anti-inflammatory effects against different models of neurodegeneration, and these effects may be employed to tackle the neurological changes. Therefore, we collected the main scientific findings and comprehensively presented them, covering preparation, absorption, and receptor-mediated functions, including effects against Alzheimer’s disease models, Parkinson’s disease models, anxiety and depression-like models, and other neurological disorders, aiming to provide some insights for the possible usage of gintonin in the management of neurodegenerative conditions.

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“…The energy-dependent absorption profile of ginsenosides in the mucosa of intestine [ 43 – 45 ], and the availability of both intact ginsenosides and their metabolites from the intestines are very low [ 39 , 46 , 47 ]. Gintonin can be absorbed into the intestine via transcellular and paracellular diffusion and the active transport process [ 48 ]. In general, the time for ginsenosides to reach maximum concentration (Tmax) in plasma is less than 2 hr, signifying that saponins are quickly absorbed and readily distributed in tissues [ 49 , 50 ].…”

Section: Pharmacokinetics Of Active Ginseng Componentsmentioning

confidence: 99%

Active ginseng components in cognitive impairment: Therapeutic potential and prospects for delivery and clinical study

et al. 2018

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Cognitive impairment is a state that affects thinking, communication, understanding, and memory, and is very common in various neurological disorders. Among many factors, age-related cognitive decline is an important area in mental health research. Research to find therapeutic medications or supplements to treat cognitive deficits and maintain cognitive health has been ongoing. Ginseng and its active components may have played a role in treating chronic disorders. Numerous preclinical studies have confirmed that ginseng and its active components such as ginsenosides, gintonin, and compound K are pharmacologically efficacious in different models of and are linked to cognitive impairment. Among their several roles, they act as an anti-neuroinflammatory and help fight against oxidative stress and modulate the cholinergic signal. These roles may be involved in enhancing cognition and attenuating impairment. There have been some clinical studies on the activity of ginseng in cognitive impairment, but many ginseng species and active compounds remain to be investigated. In addition, new formulations of active ginseng components such as nanoparticles and liposomes could be used for preclinical and clinical models of cognitive impairment. Here, we discuss the therapeutic potential of active ginseng components in cognitive impairment and their chemistry and pharmacokinetics and consider prospects for their delivery and clinical study with respect to cognitive impairment.

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Gintonin absorption in intestinal model systems

Cited by 18 publications

References 28 publications

Gintonin-mediated release of astrocytic vascular endothelial growth factor protects cortical astrocytes from hypoxia-induced cell damages

Gintonin-mediated release of astrocytic vascular endothelial growth factor protects cortical astrocytes from hypoxia-induced cell damages

Ongoing Research on the Role of Gintonin in the Management of Neurodegenerative Disorders

Active ginseng components in cognitive impairment: Therapeutic potential and prospects for delivery and clinical study

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