SHR02 Modulates Inflammatory and Oxidative Stress Responses by Inhibiting NF-κB and Activating Nrf2 in Macrophages and Dendritic Cells
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SHR02, a derivative of homoisoflavonoid, exhibits potent anti-inflammatory activity in innate immune cells. In this study, we investigated the immunomodulatory effects of SHR02 in dendritic cells (DC2.4) and macrophages (RAW 264.7) under Toll-like receptor (TLR) stimulation. SHR02 significantly suppressed the secretion of pro-inflammatory cytokines (TNF-α and IL-6), reduced nitric oxide (NO) and reactive oxygen species (ROS) production, and downregulated the expression of iNOS and COX-2. Mechanistically, SHR02 inhibited NF-κB phosphorylation in dendritic cells while enhancing Nrf2 nuclear translocation in both cell types. These findings suggest that SHR02 modulates inflammatory and oxidative responses through both NF-κB and Nrf2 signaling pathways and may serve as a promising candidate for the treatment of inflammatory disorders.
Abstract
SHR02, a derivative of homoisoflavonoid, exhibits potent anti-inflammatory activity in innate immune cells. In this study, we investigated the immunomodulatory effects of SHR02 in dendritic cells (DC2.4) and macrophages (RAW 264.7) under Toll-like receptor (TLR) stimulation. SHR02 significantly suppressed the secretion of pro-inflammatory cytokines (TNF-α and IL-6), reduced nitric oxide (NO) and reactive oxygen species (ROS) production, and downregulated the expression of iNOS and COX-2. Mechanistically, SHR02 inhibited NF-κB phosphorylation in dendritic cells while enhancing Nrf2 nuclear translocation in both cell types. These findings suggest that SHR02 modulates inflammatory and oxidative responses through both NF-κB and Nrf2 signaling pathways and may serve as a promising candidate for the treatment of inflammatory disorders.