The study of ginsenoside on PPARγ expression of mononuclear macrophage in type 2 diabetes

Ni, Haixiang; Yu, Ning-juan; Yang, Xuehui

doi:10.1007/s11033-009-9864-0

Cited by 45 publications

(22 citation statements)

References 26 publications

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“…Ot have a number of active ingredients, including anti-inflammatory (Song et al, 2009), anticancer (Chae et al, 2009), antitumor (Mochizuki et al, 1995), antidiabetic (Ni et al, 2010), antihypertensive (Stavro et al, 2005), antifatigue (Lee et al, 2005), and antioxidative effects (Liu et al, 2003). Even though the presence of a number of active ingredients in red ginseng extract is noteworthy, the level of bioavailability of those substances needs to be further improved to be utilized for human health benefit.…”

Section: Introductionmentioning

confidence: 99%

Optimized conditions to produce water-in-oil-in-water nanoemulsion and spray-dried nanocapsule of red ginseng extract

et al. 2018

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The aim of this study was to optimize conditions for producing water-in-oil-in-water (W/D/W) nanoemulsion and spray-dried nanocapsule of red ginseng extract. Based on emulsion stability and average particle size analysis, optimum conditions to produce W/D/W nanoemulsion were: ratio of core to coating material, 3:7; primary emulsifier, 10% polyglycerol polyricinoleate; ratio of W/D phase to coating material, 1.5:8.5; secondary emulsifier, 10% polyoxyethylene sorbitan monolaurate; solvent, 20% ethyl acetate; secondary coating material, 10% maltodextrin (MD). Under these optimized conditions, particle size of spray-dried nanocapsules coated with MD of red ginseng ranged from 100 nm to 500 nm, based on response surface methodology with the highest yield (up to 99.7%). Results of the present study can be used to further optimize conditions to produce W/D/W nanoemulsion and spray-dried nanocapsule of red ginseng extract.

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Section: Introductionmentioning

confidence: 99%

Optimized conditions to produce water-in-oil-in-water nanoemulsion and spray-dried nanocapsule of red ginseng extract

et al. 2018

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“…Additionally, Rg1 has been recently used to treat type 2 diabetes, as it can improve peroxisome proliferator-activated receptor γ (PPARγ) expression and lipid metabolism [18].…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rg1 Decreases Aβ1–42 Level by Upregulating PPARγ and IDE Expression in the Hippocampus of a Rat Model of Alzheimer's Disease

Quan

Wang

et al. 2013

PLoS ONE

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Background and PurposeThe present study was designed to examine the effects of ginsenoside Rg1 on expression of peroxisome proliferator-activated receptor γ (PPARγ) and insulin-degrading enzyme (IDE) in the hippocampus of rat model of Alzheimer's disease (AD) to determine how ginsenoside Rg1 (Rg1) decreases Aβ levels in AD.Experimental ApproachExperimental AD was induced in rats by a bilateral injection of 10 µg soluble beta-amyloid peptide 1–42 (Aβ1–42) into the CA1 region of the hippocampus, and the rats were treated with Rg1 (10 mg·kg−1, intraperitoneally) for 28 days. The Morris water maze was used to test spatial learning and memory performance. Hematoxylin-eosin staining was performed to analyze the hippocampal histopathological damage. Immunohistochemistry, western blotting, and real-time PCR were used to detect Aβ1–42, PPARγ, and insulin-degrading enzyme (IDE) expression in the hippocampus.Key ResultsInjection of soluble Aβ1–42 into the hippocampus led to significant dysfunction of learning and memory, hippocampal histopathological abnormalities and increased Aβ1–42 levels in the hippocampus. Rg1 treatment significantly improved learning and memory function, attenuated hippocampal histopathological abnormalities, reduced Aβ1–42 levels and increased PPARγ and IDE expression in the hippocampus; these effects of Rg1 could be effectively inhibited by GW9662, a PPARγ antagonist.Conclusions and ImplicationsGiven that PPARγ can upregulate IDE expression and IDE can degrade Aβ1–42, these results indicate that Rg1 can increase IDE expression in the hippocampus by upregulating PPARγ, leading to decreased Aβ levels, attenuated hippocampal histopathological abnormalities and improved learning and memory in a rat model of AD.

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“…The ginsenoside Rg1 has demonstrated neuroprotective capacity in cerebral ischemia [13, 20], though its molecular underpinnings have not been thoroughly understood. A report in 2010 showed that Rg1 could increase the expression of PPAR γ mRNA, encoding PPAR γ receptors involved in the regulation of a barrage of biological processes including lipid metabolism and the regulation of inflammatory and oxidative responses [12]. Additional evidence has implicated PPAR γ signaling as a contributor to the neurodegenerative processes of cerebral ischemic injury.…”

Section: Discussionmentioning

confidence: 99%

“…A study in 2010 reported that Rg1 treatment could improve the expression of PPAR γ and lipid metabolism in the treatment of Type 2 diabetes [12]. More recently, the antiapoptotic and anti-inflammatory capacity of a downstream PPAR γ effector has been reported in a rat model of cerebral ischemic injury [13].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effect of the Ginsenoside Rg1 on Cerebral Ischemic Injury In Vivo and In Vitro Is Mediated by PPARγ‐Regulated Antioxidative and Anti‐Inflammatory Pathways

Guan

Wang

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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The ginsenoside Rg1 exerts a neuroprotective effect during cerebral ischemia/reperfusion injury. Rg1 has been previously reported to improve PPARγ expression and signaling, consequently enhancing its regulatory processes. Due to PPARγ's role in the suppression of oxidative stress and inflammation, Rg1's PPARγ-normalizing capacity may play a role in the observed neuroprotective action of Rg1 during ischemic brain injury. We utilized a middle cerebral artery ischemia/reperfusion injury model in rats in addition to an oxygen glucose deprivation model in cortical neurons to elucidate the mechanisms underlying the neuroprotective effects of Rg1. We found that Rg1 significantly increased PPARγ expression and reduced multiple indicators of oxidative stress and inflammation. Ultimately, Rg1 treatment improved neurological function and diminished brain edema, indicating that Rg1 may exert its neuroprotective action on cerebral ischemia/reperfusion injury through the activation of PPARγ signaling. In addition, the present findings suggested that Rg1 was a potent PPARγ agonist in that it upregulated PPARγ expression and was inhibited by GW9662, a selective PPARγ antagonist. These findings expand our previous understanding of the molecular basis of the therapeutic action of Rg1 in cerebral ischemic injury, laying the ground work for expanded study and clinical optimization of the compound.

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The study of ginsenoside on PPARγ expression of mononuclear macrophage in type 2 diabetes

Cited by 45 publications

References 26 publications

Optimized conditions to produce water-in-oil-in-water nanoemulsion and spray-dried nanocapsule of red ginseng extract

Optimized conditions to produce water-in-oil-in-water nanoemulsion and spray-dried nanocapsule of red ginseng extract

Ginsenoside Rg1 Decreases Aβ1–42 Level by Upregulating PPARγ and IDE Expression in the Hippocampus of a Rat Model of Alzheimer's Disease

Neuroprotective Effect of the Ginsenoside Rg1 on Cerebral Ischemic Injury In Vivo and In Vitro Is Mediated by PPARγ‐Regulated Antioxidative and Anti‐Inflammatory Pathways

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