3,4,5-Tricaffeoylquinic acid may attenuate the TNF-α±- and LPS-stimulated production of inflammatory mediators in keratinocytes by suppressing the Toll-like receptor 4 expression-mediated activation of the Akt, ERK and NF-Κb pathways, it may exert an inhibitory effect against the pro-inflammatory mediator-induced skin disease.

3,4,5-Tricaffeoylquinic acid may attenuate the TNF-α±- and LPS-stimulated production of inflammatory mediators in keratinocytes by suppressing the Toll-like receptor 4 expression-mediated activation of the Akt, ERK and NF-κB pathways, it may exert an inhibitory effect against the pro-inflammatory mediator-induced skin disease.

In human keratinocytes, we investigated the effect of 3,4,5-Tricaffeoylquinic acid on the tumor necrosis factor (TNF)-α±-stimulated production of inflammatory mediators in relation to the nuclear factor (NF)-κB and cell signaling Akt, which regulates the transcription genes involved in immune and inflammatory responses. 3,4,5-Tricaffeoylquinic acid inhibited the TNF-α±-stimulated production of cytokines (IL-1β and IL-8) and chemokine (CCL17 and CCL27) in keratinocytes. Bay 11-7085 (an inhibitor of NF-κB activation) and Akt inhibitor attenuated the TNF-α±-induced formation of inflammatory mediators. 3,4,5-Tricaffeoylquinic acid, Bay 11-7085, Akt inhibitor and N-acetylcysteine inhibited the TNF-α±-induced activation of NF-κB, activation of Akt, and formation of reactive oxygen and nitrogen species. The results show that 3,4,5-Tricaffeoylquinic acid seems to attenuate the TNF-α±-stimulated inflammatory mediator production in keratinocytes by suppressing the activation of Akt and NF-κB pathways which may be mediated by reactive oxygen species[1]

86632-03-3

C34H30O15

678.59

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years