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Rhodiola‐induced anti‐adipogenic effect correlates with coordinated changes of antioxidant responses in 3T3‐L1 cells
Author(s) -
Lee Ok Hwan,
Kim Yong Ook,
Swick Jennifer,
Kim YoungCheul
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.lb397
Subject(s) - rhodiola , antioxidant , tyrosol , chemistry , mangiferin , reactive oxygen species , adipogenesis , nox4 , oxidative stress , biochemistry , nadph oxidase , superoxide dismutase , pharmacology , biology , adipose tissue , salidroside , chromatography
Adipogenesis is a key process in the development of obesity and accumulated lipids of adipose tissue in obese state generate excessive reactive oxygen species (ROS), leading to elevated systemic oxidative stress. We have shown that Rhodiola extract dose‐dependently suppressed adipogenesis and ROS level in a PPARγ‐dependent manner. Here we investigated whether the anti‐adipogenic effect of Rhodiola extract and tyrosol, a major phenolic compound present in Rhodiola , alters endogenous antioxidant enzyme responses linked to hexose monophosphate (HMP) shunt during adipogenesis. 3T3‐L1 preadipocytes were differentiated with varying concentrations of Rhodiola extract or tyrosol for up to 8 days. Treatment of Rhodiola or tyrosol significantly inhibited mRNA level and enzyme activity of glucose‐6‐phosphate dehydrogenase (G6PD), a rate‐limiting enzyme in HMP pathway. These treatments also markedly reduced mRNA expression of glutathione reductase (GR) and NADPH oxidase (NOX4), a major ROS generator in adipocytes. The inhibition of G6PD likely prevented NADPH production required for NOX4 and lipid synthesis, resulting in reduced ROS level and GR activity. However, copper‐zinc superoxide dismutase and catalase mRNAs were expressed at high levels and not significantly affected. These results indicate that Rhodiola ‐induced antioxidant effect is attributable to a phenolic tyrosol and may involve direct downregulation of PPARγ or via inhibition of HMP pathway linked to antioxidant responses in adipocytes.