Pro-Resolving Effect of Ginsenosides as an Anti-Inflammatory Mechanism of Panax ginseng

Im, Dong‐Soon

doi:10.3390/biom10030444

Cited by 120 publications

(96 citation statements)

References 76 publications

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“…Akao et al [ 16 ] investigated the absorption of CK in rat plasma, and Lee et al [ 17 ] demonstrated the absorption, distribution, and metabolism of CK in humans. CK is one of the rare ginsenosides, and it is of great interest due to its diverse biological activities and high pharmacological activities [ 18 , 19 ]. However, the minute amount of CK in ginseng cannot satisfy the needs of commercial purposes [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

Antioxidant, Anti-Inflammatory and Antithrombotic Effects of Ginsenoside Compound K Enriched Extract Derived from Ginseng Sprouts

2021

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Partially purified ginsenoside extract (PGE) and compound K enriched extract (CKE) were prepared from ginseng sprouts, and their antioxidant, anti-inflammatory and antithrombotic effects were investigated. Compared to the 6-year-old ginseng roots, ginseng sprouts were found to have a higher content of phenolic compounds, saponin and protopanaxadiol-type ginsenoside by about 56%, 36% and 43%, respectively. PGE was prepared using a macroporous adsorption resin, and compound K(CK) was converted and enriched from the PGE by enzymatic hydrolysis with a conversion rate of 75%. PGE showed higher effects than CKE on radical scavenging activity in antioxidant assays. On the other hand, CKE reduced nitric oxide levels more effectively than PGE in RAW 264.7 cells. CKE also reduced pro-inflammatory cytokines, such as tumor necrosis factor-α, interleukin (IL)-1β and IL-6 than PGE. Tail bleeding time and volume were investigated after administration of CKE at 70–150 mg/kg/day to mice. CKE administered group showed a significant increase or increased tendency in bleeding time than the control group. Bleeding volume in the CKE group increased than the control group, but not as much as in the aspirin group. In conclusion, ginseng sprouts could be an efficient source of ginsenoside, and CKE converted from the ginsenosides showed antioxidant, anti-inflammatory and antithrombotic effects. However, it was estimated that the CKE might play an essential role in anti-inflammatory effects rather than antioxidant effects.

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Section: Discussionmentioning

confidence: 99%

Antioxidant, Anti-Inflammatory and Antithrombotic Effects of Ginsenoside Compound K Enriched Extract Derived from Ginseng Sprouts

2021

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“…Effects of gintonin on cell viability against iodoacetic acid (IAA)-mediated HT22 cell death. (A) IAA-induced cell death in a dose-dependent manner in HT22 cells treated with multiple concentrations of IAA (1,3,5,10,15, and 20 μM) for 2 h. (B) Dose-dependent effect of gintonin on cell viability against IAA-mediated cell apoptosis. After treating with 5 μM IAA for 2 h, HT22 cells were exposed to various concentrations of gintonin (0.1, 0.3, 1, 3, and 10 μg/mL) for 24 h. (C) Time-dependent effect of gintonin on cell viability against IAA-mediated cell apoptosis.…”

Section: Figurementioning

confidence: 99%

Protective Effects of Gintonin on Reactive Oxygen Species-Induced HT22 Cell Damages: Involvement of LPA1 Receptor-BDNF-AKT Signaling Pathway

et al. 2021

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Gintonin is a kind of ginseng-derived glycolipoprotein that acts as an exogenous LPA receptor ligand. Gintonin has in vitro and in vivo neuroprotective effects; however, little is known about the cellular mechanisms underlying the neuroprotection. In the present study, we aimed to clarify how gintonin attenuates iodoacetic acid (IAA)-induced oxidative stress. The mouse hippocampal cell line HT22 was used. Gintonin treatment significantly attenuated IAA-induced reactive oxygen species (ROS) overproduction, ATP depletion, and cell death. However, treatment with Ki16425, an LPA1/3 receptor antagonist, suppressed the neuroprotective effects of gintonin. Gintonin elicited [Ca2⁺]i transients in HT22 cells. Gintonin-mediated [Ca2⁺]i transients through the LPA1 receptor-PLC-IP3 signaling pathway were coupled to increase both the expression and release of BDNF. The released BDNF activated the TrkB receptor. Induction of TrkB phosphorylation was further linked to Akt activation. Phosphorylated Akt reduced IAA-induced oxidative stress and increased cell survival. Our results indicate that gintonin attenuated IAA-induced oxidative stress in neuronal cells by activating the LPA1 receptor-BDNF-TrkB-Akt signaling pathway. One of the gintonin-mediated neuroprotective effects may be achieved via anti-oxidative stress in nervous systems.

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“…However, despite the promising results in preclinical models, the multidomain clinical trial MAPT study showed that PUFA supplementation had no significant effects on cognitive decline over three years in elderly people with memory complaints [ 91 ]. Another nutraceutical commonly used as a herbal medicine and food supplement given its anti-inflammatory properties is ginsenoside (ginseng saponin) [ 92 ]. Ginsenosides are amphipathic compounds, acting as partial agonists of steroid hormone receptors, regulating metabolism and inflammation [ 93 ].…”

Section: Nutraceuticals As a Treatment Of Admentioning

confidence: 99%

Can We Treat Neuroinflammation in Alzheimer’s Disease?

Sánchez-Sarasúa

Fernández-Pérez

Espinosa-Fernández

et al. 2020

IJMS

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Alzheimer’s disease (AD), considered the most common type of dementia, is characterized by a progressive loss of memory, visuospatial, language and complex cognitive abilities. In addition, patients often show comorbid depression and aggressiveness. Aging is the major factor contributing to AD; however, the initial cause that triggers the disease is yet unknown. Scientific evidence demonstrates that AD, especially the late onset of AD, is not the result of a single event, but rather it appears because of a combination of risk elements with the lack of protective ones. A major risk factor underlying the disease is neuroinflammation, which can be activated by different situations, including chronic pathogenic infections, prolonged stress and metabolic syndrome. Consequently, many therapeutic strategies against AD have been designed to reduce neuro-inflammation, with very promising results improving cognitive function in preclinical models of the disease. The literature is massive; thus, in this review we will revise the translational evidence of these early strategies focusing in anti-diabetic and anti-inflammatory molecules and discuss their therapeutic application in humans. Furthermore, we review the preclinical and clinical data of nutraceutical application against AD symptoms. Finally, we introduce new players underlying neuroinflammation in AD: the activity of the endocannabinoid system and the intestinal microbiota as neuroprotectors. This review highlights the importance of a broad multimodal approach to treat successfully the neuroinflammation underlying AD.

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Pro-Resolving Effect of Ginsenosides as an Anti-Inflammatory Mechanism of Panax ginseng

Cited by 120 publications

References 76 publications

Antioxidant, Anti-Inflammatory and Antithrombotic Effects of Ginsenoside Compound K Enriched Extract Derived from Ginseng Sprouts

Antioxidant, Anti-Inflammatory and Antithrombotic Effects of Ginsenoside Compound K Enriched Extract Derived from Ginseng Sprouts

Protective Effects of Gintonin on Reactive Oxygen Species-Induced HT22 Cell Damages: Involvement of LPA1 Receptor-BDNF-AKT Signaling Pathway

Can We Treat Neuroinflammation in Alzheimer’s Disease?

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