OBJECTIVE: An ethanolic extract of Artemisia scoparia (SCO) improves adipose tissue function and reduces negative metabolic consequences of high-fat feeding. A. scoparia has a long history of medicinal use across Asia and has anti-inflammatory effects in various cell types and disease models. The objective of the current study was to investigate SCO's effects on inflammation in cells relevant to metabolic health. METHODS: Inflammatory responses were assayed in cultured adipocytes, macrophages, and insulinoma cells by quantitative polymerase chain reaction, immunoblotting, and NF-κB reporter assays. RESULTS: In tumor necrosis factor α-treated adipocytes, SCO mitigated ERK and NF-κB signaling as well as transcriptional responses but had no effect on fatty acid-binding protein 4 secretion. SCO also reduced levels of deleted in breast cancer 1 protein in adipocytes and inhibited inflammatory gene expression in stimulated macrophages. Finally, in pancreatic β-cells, SCO decreased NF-κB-responsive promoter activity induced by IL-1β treatment. CONCLUSIONS: SCO's ability to promote adipocyte development and function is thought to mediate its insulin-sensitizing actions in vivo. Our findings that SCO inhibits inflammatory responses through at least two distinct signaling pathways (ERK and NF-κB) in three cell types known to contribute to metabolic disease reveal that SCO may act more broadly than previously thought to improve metabolic health.
OBJECTIVE: An ethanolic extract of Artemisia scoparia (SCO) improves adipose tissue function and reduces negative metabolic consequences of high-fat feeding. A. scoparia has a long history of medicinal use across Asia and has anti-inflammatory effects in various cell types and disease models. The objective of the current study was to investigate SCO's effects on inflammation in cells relevant to metabolic health. METHODS: Inflammatory responses were assayed in cultured adipocytes, macrophages, and insulinoma cells by quantitative polymerase chain reaction, immunoblotting, and NF-κB reporter assays. RESULTS: In tumor necrosis factor α-treated adipocytes, SCO mitigated ERK and NF-κB signaling as well as transcriptional responses but had no effect on fatty acid-binding protein 4 secretion. SCO also reduced levels of deleted in breast cancer 1 protein in adipocytes and inhibited inflammatory gene expression in stimulated macrophages. Finally, in pancreatic β-cells, SCO decreased NF-κB-responsive promoter activity induced by IL-1β treatment. CONCLUSIONS: SCO's ability to promote adipocyte development and function is thought to mediate its insulin-sensitizing actions in vivo. Our findings that SCO inhibits inflammatory responses through at least two distinct signaling pathways (ERK and NF-κB) in three cell types known to contribute to metabolic disease reveal that SCO may act more broadly than previously thought to improve metabolic health.
Authors: Anik Boudreau; Alexander Poulev; David M Ribnicky; Ilya Raskin; Thirumurugan Rathinasabapathy; Allison J Richard; Jacqueline M Stephens Journal: Front Nutr Date: 2019-03-08
Authors: Allison J Richard; Scott Fuller; Veaceslav Fedorcenco; Robbie Beyl; Thomas P Burris; Randall Mynatt; David M Ribnicky; Jacqueline M Stephens Journal: PLoS One Date: 2014-06-10 Impact factor: 3.240
Authors: Laura M Mongioì; Sandro La Vignera; Rossella Cannarella; Laura Cimino; Michele Compagnone; Rosita A Condorelli; Aldo E Calogero Journal: Int J Mol Sci Date: 2021-04-22 Impact factor: 5.923