10.6084/m9.figshare.7593068.v1 Ding J. Ding J. Luo C. Luo C. Wang X. Wang X. Zhou T. Zhou T. Zheng X. Zheng X. Zhang Z. Zhang Z. Yu B. Yu B. Zhang J. Zhang J. Tong X. Tong X. Supplementary Material for: Glycyrrhizin, a High-Mobility Group Box 1 Inhibitor, Improves Lipid Metabolism and Suppresses Vascular Inflammation in Apolipoprotein E Knockout Mice Karger Publishers 2019 Atherosclerosis Glycyrrhizin High-mobility group box protein 1 Regulatory T cell T helper cell 17 2019-01-16 09:07:48 Dataset https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Glycyrrhizin_a_High-Mobility_Group_Box_1_Inhibitor_Improves_Lipid_Metabolism_and_Suppresses_Vascular_Inflammation_in_Apolipoprotein_E_Knockout_Mice/7593068 <b><i>Background:</i></b><i></i> High-mobility group box protein 1 (HMGB1) is known to have proinflammatory properties;<i></i> however, the mechanisms by which HMGB1 influences immune responses during atherosclerosis (AS) development are not well understood. Thus, this study investigated the relationship between HMGB1 and vascular inflammation in <i>Apoe</i><sup><i>–/–</i></sup> mice and whether glycyrrhizin (GLY), a small inhibitor of HMGB1, could have atheroprotective effects in AS. <b><i>Methods:</i></b> <i>Apoe</i><sup><i>–/–</i></sup> mice on a high-fat diet were treated with GLY (50 mg/kg) or vehicle by gavage once daily for 12 weeks, respectively. <b><i>Results:</i></b><i></i> The GLY group exhibited significantly decreased serum lipid levels, atherosclerotic plaque deposition, and serum HMGB1 levels, as well as an increased Treg/Th17 ratio. The GLY group displayed increased interleukin-10 (IL-10) and IL-2 expression and decreased IL-17A and IL-6 expression. Furthermore, the GA treatment significantly reduced STAT3 phosphorylation in Th17 cells and increased STAT5 phosphorylation in Treg cells. <b><i>Conclusions:</i></b> Our findings indicate that the attenuation of atherosclerotic lesions in <i>Apoe</i><sup><i>–/–</i></sup> mice by GLY might be associated with the amelioration of lipid metabolism abnormalities, inhibition of HMGB1 expression, and alterations in the Treg/Th17 ratio.