Abstract
CAPE is known as an antioxidant, and it is proposed that the induction of HO-1 by CAPE is mediated by a redox-regulated mechanism. Therefore in this study we examined whether the activation of HO-1 gene by CAPE is dependent upon redox mechanisms. RAW cells were incubated with (1) CAPE, (2) caffeic acid ethyl ester (CAEE), (3) chlorogenic acid or (4) curcumin for 4 hrs. and mRNA of HO-1 gene was measured by RT-PCR. As a result the mRNA was enhanced by the chemicals as (1) 36.5, (2) 20.1, (3) 1.3 and (4) 6.4 times respectively. Then to measure reductive activities each chemical was subjected to the second-harmonic alternative current voltammetry. The one-electron oxidation potentials of these phenolic compounds were 0.48 (CAPE), 0.49 (CAEE), 0.48 (chlorogenic acid) and 0.42 (curcumin). Thus curcumin exhibited the highest reductive activity, and the others were less potent and almost at the same level. However the increase of HO-1 mRNA by curcumin was less than CAPE in spite of its higher reductive capacity, and also chlorogenic acid exhibited little activation of HO-1 gene in spite of the same level of reductive capacity as CAPE. When we compare the structure of CAPE and chlorogenic acid, it is presumed that a big substituent of chlorogenic acid might interrupt the interaction with cellular components but not in CAPE. From these results we suggest that the transcriptional activation of HO-1 gene by CAPE and CAEE is not dependent on a redox-regulated mechanism, but on a structure-specific interaction mediated by receptors.
