2018
DOI: 10.1016/j.biopha.2018.09.169
|View full text |Cite
|
Sign up to set email alerts
|

Red ginseng-derived saponin fraction suppresses the obesity-induced inflammatory responses via Nrf2-HO-1 pathway in adipocyte-macrophage co-culture system

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

0
15
0

Year Published

2019
2019
2023
2023

Publication Types

Select...
7

Relationship

1
6

Authors

Journals

citations
Cited by 26 publications
(15 citation statements)
references
References 41 publications
0
15
0
Order By: Relevance
“…Ginsenoside Re enhanced the activation of Nrf2 in Aβ-induced SH-SY5Y cells [76]. The activation of the Nrf2-HO-1 pathway for M2 macrophage polarization is also supported by the findings that a red ginseng-derived saponin fraction suppressed inflammatory responses via the Nrf2-HO-1 pathway in an adipocyte-macrophage co-culture system [42], and that saponins from Panax notoginseng acted as an extrinsic regulator that activates the Nrf2 antioxidant defense system and inhibits NF-κB inflammatory signaling to attenuate LPS-induced monocyte adhesion on cerebral endothelial cells [77].…”
Section: Perspectivementioning
confidence: 65%
See 1 more Smart Citation
“…Ginsenoside Re enhanced the activation of Nrf2 in Aβ-induced SH-SY5Y cells [76]. The activation of the Nrf2-HO-1 pathway for M2 macrophage polarization is also supported by the findings that a red ginseng-derived saponin fraction suppressed inflammatory responses via the Nrf2-HO-1 pathway in an adipocyte-macrophage co-culture system [42], and that saponins from Panax notoginseng acted as an extrinsic regulator that activates the Nrf2 antioxidant defense system and inhibits NF-κB inflammatory signaling to attenuate LPS-induced monocyte adhesion on cerebral endothelial cells [77].…”
Section: Perspectivementioning
confidence: 65%
“…For the mechanism of ginseng anti-inflammation, several targets were proposed: (1) activation of the glucocorticoid receptor, the target of steroidal anti-inflammatory drugs such as cortisol and dexamethasone (compound K, ginsenosides Rg1 and Re) [36][37][38][39]; (2) an anti-oxidation-related mechanism, i.e., inhibition of ROS production and activation of Nrf-2 and HO-1 (compound K, ginsenosides Rg1, Rb1, Ro, and Rg5) [27,33,36,[40][41][42]; (3) blocking of TLR4 interaction with LPS (ginsenosides Re and Rg5) [43,44]; (4) activation of anti-inflammatory PPARγ (ginsenosides Rg3, Re, Rb1, Rg1, and Rf) [40,[45][46][47][48][49][50].…”
Section: Ginsenosides In Anti-inflammationmentioning
confidence: 99%
“…HO-1 upregulation has also been linked to increased insulin sensitivity, improvement in phosphorylation of insulin receptors, and improved adipocyte function [35]. Previously published studies have shown the protective role of HO-1 in inhibiting the inflammatory effect of several mediators; inflammatory and oxidative transcription factors, such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κβ) and c-Jun N-terminal kinase (JNK), which are primarily involved in inflammatory insult, stimulate inflammatory pathways, creating a feedback mechanism of inflammation [35,54,56]. Evidence from the literature suggests a potential interaction between HO-1 and adiponectin.…”
Section: The Na/k-atpase Oxidant Amplification Loop and Ho-1: Implicamentioning
confidence: 99%
“…Cobalt protoporphyrin (CoPP) is an exogenous inducer of HO-1 that theoretically acts through the FoxO1 protein [54,56,69]. Current literature hypothesizes that FoxO1 negatively regulates adipogenesis by preventing transcription of PPARγ; decreased adipogenesis leads to a decrease in systemic oxidative stress and inflammatory cytokines [36,56].…”
Section: Approaches To Targeted Upregulation Of Ho-1mentioning
confidence: 99%
See 1 more Smart Citation