Visfatin is regulated by interleukin-6 and affected by the PPAR-γ pathway in BeWo cells

Visfatin, an adipocytokine and cytosolic enzyme with nicotinamide phosphoribosyltransferase (Nampt) activity, is involved in the pathogenesis of numerous metabolic disorders. In addition, the nuclear receptor peroxisome proliferator-activated receptor-γ (PPAR-γ) serves important roles in anti-inflammatory reactions and regulates glucose and lipid metabolism. The aim of the present study was to investigate the effect of interleukin-6 (IL-6) on the expression and secretion of visfatin in BeWo cells, and to determine whether the PPAR-γ pathway is involved in the regulation of visfatin by IL-6. Therefore, BeWo cells were stimulated with serial concentrations of IL-6 or pioglitazone, and the expression levels of visfatin and PPAR-γ were determined by reverse transcription-quantitative polymerase chain reaction and western blotting. The results of the present study demonstrated that IL-6 downregulated the mRNA levels of visfatin and PPAR-γ, which were strongly associated. Activation of PPAR-γ by pioglitazone resulted in significantly increased expression of visfatin, which abrogated the inhibitory effect of IL-6 on visfatin in BeWo cells. Furthermore, treatment using pioglitazone alone increased the expression and secretion of the visfatin protein, compared with the control or IL-6 alone group. In summary, the findings of the present study suggested that IL-6 inhibited the expression of visfatin and PPAR-γ at the transcriptional level; in addition, activation of PPAR-γ upregulated visfatin at the mRNA and protein expression levels. Therefore, the PPAR-γ signaling pathway may be involved in the regulation of visfatin by IL-6 in BeWo cells. These results may provide novel insight into the roles of visfatin in trophoblastic cells. Furthermore, thiazolidinedione pioglitazone, by upregulating visfatin expression, may promote the energy metabolism of trophoblastic cells, maintain the function of the placenta and improve the outcome of pregnancy.