2011
DOI: 10.1016/j.fitote.2011.05.005
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Ginsenoside Rh1 inhibits the invasion and migration of THP-1 acute monocytic leukemia cells via inactivation of the MAPK signaling pathway

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Cited by 28 publications
(23 citation statements)
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“…G-Rh1 at the concentrations of 10 and 20 µM significantly attenuated the toxicity on SH-SY5Y cells exposed to 60 µM of sixhydroxydopamine. This was partially because of the reduction of ERK1/2 phosphorylation by G-Rh1 pretreatment, as could be seen in other cell lines such as HepG2, U87MG, U937, and THP-1 cells [21,23,30,40]. G-Rh1 increased the percentage of PC-12 cells with neurites compared to that of the control.…”
Section: Effect On Nervous Systemssupporting
confidence: 52%
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“…G-Rh1 at the concentrations of 10 and 20 µM significantly attenuated the toxicity on SH-SY5Y cells exposed to 60 µM of sixhydroxydopamine. This was partially because of the reduction of ERK1/2 phosphorylation by G-Rh1 pretreatment, as could be seen in other cell lines such as HepG2, U87MG, U937, and THP-1 cells [21,23,30,40]. G-Rh1 increased the percentage of PC-12 cells with neurites compared to that of the control.…”
Section: Effect On Nervous Systemssupporting
confidence: 52%
“…In addition, G-Rh1 markedly suppressed the CXCL-10 expression in TNF-α-induced human promonocytic U937 cells, which may be related to the inactivation of the ERK1/2 signaling pathway [40]. In THP-1 cells, G-Rh1 did not only inactivate ERK1/2, but also attenuated the phosphorylation and activation of MAPK signaling, p38MAPK and JNK activation of PKB/Akt through lowering the expression of MCP-1 and CCR2, and deactivating integrins, the fibronectin receptor VLA-5 and CD29 [21]. Li et al [22] found that after long-term dexamethasone treatment in RAW264.7 cells, it also induced the activation of DUSP1, resulting in the downregulation of proinflammatory cytokines (IL-6, IL-17, MMP-1, TNF-α).…”
Section: Anticancer Effectsmentioning
confidence: 96%
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“…For monocyte migration to occur integrins must be activated to provide docking sites at the blood-epithelial cell barrier. 19,20 Interestingly, the AQ ginseng extract downregulated two integrins: integrin alpha 8 and integrin, beta-like 1. This would suggest that polysaccharides in ginseng may trigger an inflammatory response in differentiated preadipocytes, but simultaneously prevent macrophage adhesion; however, this can only be elucidated by using a co-culture experimental system.…”
mentioning
confidence: 99%
“…The regulation of adipocyte integrins may offer a partial explanation for the previously reported whole-body anti-inflammatory effects in mice and humans treated with various ginsenosides. 20,21 More importantly, it suggests further research is needed to determine if ginseng is stimulating a local inflammatory event in adipocytes or, alternatively, whether adipocytes are contributing to an overall systemic response.…”
mentioning
confidence: 99%