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Pro-inflammatory cytokines (e.g., IL-1 and TNF), mediators of Th1 and Th17 cells (e.g., IFN and IL-17), and effector mechanisms involving neutrophils, macrophages, and plasma cells are all implicated in the disease process [28, 29]

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In addition, both hematoxylin-and-eosin staining of heart, liver, spleen, lung, and kidney and analysis of blood levels of alanine aminotransferase, aspartate aminotransferase, blood urea nitrogen, creatinine, alkaline phosphatase, and uric acid revealed no obvious pathological or functional changes among the various treatment groups (Supplementary Figs

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