|Abstract||NF-kB is a key regulator of inflammatory signaling in the cell and is a transcription factor for many genes, including interferon-beta. The constitutive activation of NF-kB can cause hyperinflammation, which is implicated in many diseases, including rheumatoid arthritis and inflammatory bowel disease. Many anti-inflammatory drugs and compounds, such as diclofenac, and curcumin, have been found to inhibit NF-kB activation, thus blocking the inflammatory response. Treatment for inflammatory disorders has also included Equisetum arvense (common Horsetail) as an herbal remedy for arthritis. Since plant extracts of E. arvense have been shown to exhibit medicinal, anti-inflammatory properties, we wanted to investigate the effect of an E. arvense extract on NF-kB signaling by looking at the TNFa-mediated activation of the NF-kB promoter and comparing the anti-inflammatory effects of the extract with diclofenac and curcumin. We first show that diclofenac, curcumin, and the E. arvense extract all inhibit TNFa-induced NF-kB activation. We then show that treatment of cells with TNFa, a known stimulator of NF-kB mediated inflammation, leads to the activation of NF-kB specific promoters, and that this activation is mitigated by the transfection of cells with IkBDN. Our results suggest that the anti-inflammatory effects of Equisetum arvense may act via the modulation of similar signaling pathways as other commercial anti-inflammatory drugs.