An ethanolic extract of Artemisia scoparia (SCO) has previously been shown to enhance differentiation of 3T3-L1 adipocytes and to have metabolically favorable effects in a mouse model of diet-induced obesity. SCO also attenuates tumor necrosis alpha (TNFa)-induced lipolysis in cultured murine adipocytes. In obesity, the infiltration of pro-inflammatory macrophages and other immune cells contributes to adipocyte dysfunction and whole-body metabolic dysregulation. Given the importance of adipose tissue inflammation in obesity and insulin resistance, we examined whether SCO could attenuate inflammatory processes in cultured macrophages and adipocytes.
Inflammatory responses were elicited with lipopolysaccharide (LPS) in RAW 264.7 macrophages, and with TNFa in 3T3-L1 adipocytes. Changes in expression of inflammatory genes were assessed using RT-qPCR, while immunoblotting was used to examine phospho-activation and nuclear translocation of the pro-inflammatory transcription factor NF-kB.
In macrophages, pretreatment with SCO greatly inhibited LPS-induced expression of inducible nitric oxide synthase (Nos2) and interleukin 1-beta, but not that of Tnfa. In 3T3-L1 adipocytes, SCO pretreatment attenuated the inflammatory response elicited by TNFa, as measured by changes in expression of monocyte chemoattractant protein-1 and interleukin 6. SCO also reduced TNFa-induced phosphorylation and nuclear translocation of the p65 subunit of NF-kB, steps that drive transcriptional activation of pro-inflammatory genes.
Our data indicate that SCO’s anti-inflammatory actions may modulate cross-talk between adipocytes and immune cells in a manner that provides metabolic protection in the context of obesity and insulin resistance. Ongoing research in our lab is focused on further mechanistic studies, as well as activity-guided fractionation of SCO to identify compounds responsible for its anti-inflammatory effects.