The inhibition of inflammatory molecule expression on 3T3-L1 adipocytes by berberine is not mediated by leptin signaling.
- Author:
Bong Hyuk CHOI
1
;
Yu Hee KIM
;
In Sook AHN
;
Jung Heun HA
;
Jae Min BYUN
;
Myoung Sool DO
Author Information
- Publication Type:Original Article
- Keywords: Berberine; inflammation; STAT-3; I-kappaB phosphorylation; 3T3-L1 adipocytes
- MeSH: Adipocytes; Adipokines; Berberine; Blotting, Western; Down-Regulation; Inflammation; Leptin; NF-kappa B; Phosphorylation; Signal Transduction; Transcription Factors
- From:Nutrition Research and Practice 2009;3(2):84-88
- CountryRepublic of Korea
- Language:English
- Abstract: In our previous study, we have shown that berberine has both anti-adipogenic and anti-inflammatory effects on 3T3-L1 adipocytes, and the anti-adipogenic effect is due to the down-regulation of adipogenic enzymes and transcription factors. Here we focused more on anti-inflammatory effect of berberine using real time RT-PCR and found it changes expressions of adipokines. We hypothesized that anti-adipogenicity of berberine mediates anti-inflammtory effect and explored leptin as a candidate mediator of this signaling. We studied this hypothesis by western blot analysis, but our results showed that berberine has no effect on the phosphorylations of STAT-3 and ERK which have important roles on leptin signaling. These results led us to conclude that the anti-inflammatory effect of berberine is not mediated by the inhibition of leptin signal transduction. Moreover, we have found that berberine down-regulates NF-kappaB signaling, one of the inflammation-related signaling pathway, through western blot analysis. Taken together, the anti-inflammatory effect of berberine is not mediated by leptin, and berberine induces anti-inflammatory effect independent of leptin signaling.
