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This hypercatabolism is evident by our data demonstrating depletion of amino acids and upregulation of the urea cycle as judged by elevated levels of urea cycle metabolites such as citrulline
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2D–F, dose-dependent treatment with SP reduced the proportions of M1-like macrophages as well as increased the proportions of anti-inflammatory M2-like macrophages (mannose receptor CD206 as the phenotypic marker of M2-like macrophages), suggesting that SP inhibited the polarization of proinflammatory M1-like macrophages and promoted the differentiation of anti-inflammatory M2-like macrophages
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