Schisandrin C attenuates renal damage in diabetic nephropathy by regulating macrophage polarization

白细胞介素 糖尿病肾病 肿瘤坏死因子α 巨噬细胞极化 药理学 STAT蛋白 化学 医学 车站3 内分泌学 细胞凋亡 内科学 细胞因子 巨噬细胞 体外 生物化学
作者
Yu Wang,Jingqiu Cui,Ming Liu,Yingqi Shao,Xiaoying Dong
出处
期刊:American Journal of Translational Research [e-Century Publishing Corporation]
卷期号:13 (1): 210-222 被引量:12
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摘要

This study aimed to investigate the protective effects of Schisandrin C during diabetic nephropathy (DN) treatment. After DN induction, mice were treated with Schisandrin C, and diabetic metabolic parameters and renal function-associated factors were measured. Renal structural damage was evaluated by hematoxylin and eosin (HE) and Masson's trichrome staining. Macrophage polarization and macrophage-mediated inflammatory factors were detected in the kidneys by immunohistochemistry (IHC) and enzyme-linked immunosorbent assay (ELISA), respectively. The Swiprosin-1/interferon (IFN)-γ-Rβ pathway was evaluated by western blot (WB) analysis. The preliminary effects of Schisandrin C in high-glucose-stimulated macrophages from DN mice were verified by flow cytometry, ELISA, and WB analyses. These results indicated that Schisandrin C significantly regulated physiological parameters in DN. Renal structural damage was mitigated by Schisandrin C. In Schisandrin-C-treated groups, the expression levels of CD86, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β decreased, whereas CD206, IL-10, and transforming growth factor (TGF)-β expression levels increased. In vitro experiments indicated that among CD86+ cells, TNF-α, IL-6, and IL-1β expression levels significantly decreased, whereas among CD206+ cells, IL-10 and TGF-β expression increased following Schisandrin-C-treatment. Finally, Schisandrin C inhibited the expression of Swiprosin-1, IFN-γ-Rβ, phospho-Janus kinase 2 (p-JAK2), phospho-signal transducer and activator of transcription 1 (p-STAT1), and p-STAT3, in both DN model mice and high-glucose-stimulated RAW264.7 cells. The present study indicated a novel use for Schisandrin C to suppress DN progression, by promoting M1 to M2 macrophage polarization. Schisandrin C exerted protective effects against DN by regulating the polarization-dependent Swiprosin-1/IFN-γ-Rβ signaling pathway in macrophages.
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