Table 5.

Overview on the interference of chromenols with molecular targets and key enzymes connecting inflammation and carcinogenesis.

NF-кB				MAPKs
Sargachromenol
TNF-α p65 Trl HUVEC 40 µM inhibition (Gwon et al., 2017)	TNF-α p65 PE HUVEC 40 µM inhibition (Gwon et al., 2017)	LPS p65 Trl BV-2 60 µM inhibition (Kim et al., 2014)	TNF-α IкB-α Phos HUVEC 40 µM inhibition (Gwon et al., 2017)	LPS JNK Phos BV-2 60 µM inhibition (Kim et al., 2014)	LPS p38 Phos BV-2 60 µM no inhibition (Kim et al., 2014)	LPS ERK Phos BV-2 60 µM inhibition (Kim et al., 2014)
TNF-α IкB-α Phos HUVEC 40 µM inhibition (Gwon et al., 2017)	LPS IкB-α Phos BV-2 60 µM inhibition (Kim et al., 2014)

The content of each cell of the table is constructed as follows (read from top to bottom): (i) used stimulus; (ii) investigated parameter; (iii) cell type tissue, mouse, or other models used for the studies; (iv) used concentration of the respective compound; (v) observed effect on the studied parameter; (vi) reference. The following abbreviations are used. BV-2, brain microglial cells transformed by recombinant retrovirus (v-raf/v-mic); JNK, c-Jun N-terminal kinase; ERK, extracellular-signal regulated kinase; HUVEC, human umbilical vein endothelial cells; LPS, lipopolysaccharide; NF-кB, nuclear factor kappa-light-chain-enhancer of activated B cells; p65, nuclear factor NF-кB p65 subunit; IкB, nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor; Phos, phosphorylation; PE, protein expression; Trl, translocation; TNF-α, tumor necrosis factor α.