Methazolamide can treat atherosclerosis. Methazolamide can treat atherosclerosis

Methoxazolamide (MTZ) has been confirmed to treat atherosclerosis (AS) by inhibiting calcification in aortic tissues. This study investigated the therapeutic mechanism. In this study, ApoE-/- mice were fed a high-fat diet to establish an AS model and then treated with MTZ. The aortic tissues were analyzed using single-cell sequencing. MTZ significantly increased the proportions of B-1/MZB cells, CD8+CD122+ Treg-like cell. Those cells can exert atheroprotective role by suppressing immune response and proinflammation. Meanwhile, MTZ decreased the proportions of nonclassical CD14+CD16++ monocytes and Spp1+ macrophages. Those cells can exert atherogenic role by suppressing proinflammation, calcification and tissue remodeling. The result suggested that MTZ is a potential anti-AS drug that regulates proportions of immunosuppressive cells and proinflammatory cells as well as their calcification-stimulating gene expression. Overall design: ApoE-/- mice were fed a high-fat diet to establish an AS model and then treated with MTZ. The aortic tissues were analyzed using single-cell sequencing.

甲氧唑酰胺（Methoxazolamide, MTZ）已被证实可通过抑制主动脉组织钙化治疗动脉粥样硬化（atherosclerosis, AS）。本研究对其治疗机制展开探究。本研究采用高脂膳食喂养载脂蛋白E敲除（ApoE-/-）小鼠以构建动脉粥样硬化模型，随后给予MTZ干预。通过单细胞测序对小鼠主动脉组织进行分析后发现，MTZ可显著提升B-1/边缘区B细胞（B-1/MZB cells）、CD8+CD122+调节性T细胞样细胞的比例；此类细胞可通过抑制免疫应答与促炎反应发挥抗动脉粥样硬化作用。与此同时，MTZ可降低非经典CD14+CD16++单核细胞与骨桥蛋白阳性（Spp1+）巨噬细胞的比例；此类细胞可通过促进促炎反应、钙化及组织重塑发挥致动脉粥样硬化作用。研究结果表明，MTZ是一种潜在的抗动脉粥样硬化药物，可调节免疫抑制细胞与促炎细胞的比例，并调控其钙化相关基因的表达。整体实验设计：采用高脂膳食喂养ApoE-/-小鼠构建动脉粥样硬化模型，随后给予MTZ干预，并通过单细胞测序对主动脉组织进行分析。