Caffeic acid phenethyl ester suppresses oxidative stress in 3T3-L1 adipocytes

Abstract

The generation of oxidative stress, characterized by enhanced reactive oxygen species (ROS) formation, has been found in obesity. ROS production was increased during the differentiation of 3T3-L1 cells into adipocytes. We previously reported that caffeic acid phenethyl ester (CAPE) suppresses 3T3-L1 differentiation to adipocytes through the inhibition of peroxisome proliferator-activated receptor γ. In this study, the preventive effect of CAPE on oxidative stress in 3T3-L1 cells was observed. The results were as follows: (1) ROS production during 3T3-L1 cell differentiation to adipocytes was significantly (p < 0.05) suppressed by CAPE treatment in a concentration-dependent manner, (2) with CAPE treatment, the extracellular superoxide dismutase mRNA expression level significantly increased, but the NOX4 mRNA expression level did not change, and (3) CAPE treatment significantly increased superoxide dismutase (SOD) activity in 3T3-L1 cells. From these results, we suggest that the increased oxidative stress in 3T3-L1 differentiation to adipocytes is attenuated by CAPE treatment. This attenuation may be partly caused by increased SOD production.

Nrf2-Mediated HO-1 Induction Coupled with the ERK Signaling Pathway Contributes to Indirect Antioxidant Capacity of Caffeic Acid Phenethyl Ester in HepG2 Cells

“…This inducing effect of antioxidant-related gene by CAPE has been confirmed through studies with human umbilical vein endothelial cells that showed that CAPE suppressed menadione-induced oxidative stress by inducing HO-1 gene [22,23] and with porcine renal epithelial cells showed that CAPE significantly increased HO-1 protein expression through stimulating Nrf2 expression [19]. The inducing effect of CAPE on phase II antioxidant and detoxifying enzymes such as HO-1 and superoxide dismutase (SOD) has also been identified in different types of cells such as astrocytes [24], hippocampal neurons [25], macrophage cells [26], and 3T3-L1 adipocytes [27]. Accordingly, the above results suggest that CAPE can exert potent intracellular antioxidant activity by inducing HO-1 expression.…”

Administration of Purwoceng (<I>Pimpinella alpina</I> Molk) Improves Oxidative Stress Biomarker Following UVC Irradiation in Spargue-Dawley Male Rats

“…Concomitantly, treatment of caffeic acid phenethyl ester (flavonoid) also significantly increased superoxide dismutase (SOD) activity in 3T3-L1 cells. Based on these results, the authors conclude that flavonoid can attenuate oxidative stress in 3T3-L1 differentiation to adipocytes, mediated partly by increased SOD production 39 . The later study is in agreement with the present study; PaM treatment was able to decrease MDA level and concurrently increased TAC level of plasma.…”

“…The limitation in the Li 38 study didn't investigate either TAC or antioxidant enzymes such as SOD, Cat, and GPx, accordingly could not evaluate prooxidant and antioxidant balance status. However, this limitation was answered by another in-vitro study carried out by Yasui et al 39 .This study pointed out that caffeic acid phenethyl ester (CAPE), a type of flavonoid ascribe to propolis was proven to suppress ROS production assessed by nitrobluetetrazolium (NBT) in 3T3-L1 cell during differentiation to adipocytes significantly in a concentration-dependent manner. Concomitantly, treatment of caffeic acid phenethyl ester (flavonoid) also significantly increased superoxide dismutase (SOD) activity in 3T3-L1 cells.…”

Caffeic Acid Phenethyl Ester and Therapeutic Potentials

“…Large research has been done to assess antioxidant role of CAPE [10, 86]. The evidences show that CAPE is potent antioxidant which can scavenge ROS and protect the cell membrane against lipid peroxidation [87–91]. Some other studies elaborate immunomodulator [4, 38, 92], antihepatotoxic [93], antiosteogenic [94], and antiatherosclerotic [95] (Table 1) role of CAPE.…”