2019
DOI: 10.1016/j.biopha.2019.109066
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Korean red ginseng water extract alleviates atopic dermatitis-like inflammatory responses by negative regulation of mitogen-activated protein kinase signaling pathway in vivo

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Cited by 22 publications
(13 citation statements)
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“…Previous studies have shown that the antifibrosis effect of a type of ginsenoside AD-2 extracted from ginseng on thioacetamide-induced liver injury in mice is related to the inflammatory factors (including TNF- α , IL-1 β , caspase-1, and IL-6) associated with hepatic fibrosis [ 32 ]. Korean red ginseng water extract decreased the mRNA expression levels of interleukin-6 (IL-6), thymic stromal lymphopoietin (TSLP), and TNF- α in the 1-chloro-2,4-dinitrobenzene- (DNCB-) induced BALB/c mouse model which develops atopic dermatitis- (AD-) like lesions and alleviates AD-like inflammatory responses [ 33 ]. For liver fibrosis in rats induced by CCl 4 , ginseng extract inhibits liver inflammation by downregulating rat hepatic prostaglandin E 2 and tissue inhibitor metalloproteinase-1 (TIMP-1) [ 34 ].…”
Section: Discussionmentioning
confidence: 99%
“…Previous studies have shown that the antifibrosis effect of a type of ginsenoside AD-2 extracted from ginseng on thioacetamide-induced liver injury in mice is related to the inflammatory factors (including TNF- α , IL-1 β , caspase-1, and IL-6) associated with hepatic fibrosis [ 32 ]. Korean red ginseng water extract decreased the mRNA expression levels of interleukin-6 (IL-6), thymic stromal lymphopoietin (TSLP), and TNF- α in the 1-chloro-2,4-dinitrobenzene- (DNCB-) induced BALB/c mouse model which develops atopic dermatitis- (AD-) like lesions and alleviates AD-like inflammatory responses [ 33 ]. For liver fibrosis in rats induced by CCl 4 , ginseng extract inhibits liver inflammation by downregulating rat hepatic prostaglandin E 2 and tissue inhibitor metalloproteinase-1 (TIMP-1) [ 34 ].…”
Section: Discussionmentioning
confidence: 99%
“…MAPK signaling pathways are significant mechanisms in inflammatory responses. It is reported that increased phosphorylation and activation of ERK, JNK, and p38 in AD mice and keratinocytes are a result of the inflammatory response in AD [29,30]. This study showed that the DfE-induced phosphorylation of ERK, JNK, and p38 was decreased by NHGR treatment.…”
Section: Discussionmentioning
confidence: 48%
“…Filaggrin expression decreased by TNF-α and IFN-γ is related to activation of JNK, and CS stimulation increased filaggrin expression by blocking activation of JNK in contrast to other reports ( Figs. 1 and 4) [25,26]. These results indicate that JNK is a key molecule that controls filaggrin expression.…”
Section: Discussionmentioning
confidence: 68%