Excess weight and obesity increase the risk of developing major risk factors for chronic kidney disease. Lignin comprises 20%-30% of the global plant biomass; however, it is not well utilized because of its resistance to chemical and biological degradation. We investigated whether low-molecular-weight oxidized lignophenol (LOLP), a lignin derivative, could alter inflammation and fibrosis in the kidneys of a high-fat diet (HFD)-fed mice. Male mice were divided into three treatment groups: HFD; HFD +0.3% LOLP; and HFD +0.6% LOLP. The control mice (Cont) were fed a low-fat diet. Macrophage kinetics, the degree of fibrosis, the extent of phosphorylation of AMP-activated protein kinase (AMPK), and mRNA expression of proinflammatory mediators in the kidneys were examined. The number of macrophages, the percentage of fibrotic area, and the mRNA expression of proinflammatory markers, TNF-α and Ccl2, and a marker of fibrosis, TGF-β, were significantly higher in the kidneys of mice in the HFD group than those in the Cont group. Conversely, treatment with 0.6% LOLP for 8 weeks significantly suppressed the degree of macrophage infiltration, interstitial fibrotic area, and the increased mRNA expression of proinflammatory and fibrosis markers induced by HFD. In conclusion, LOLP suppressed macrophage infiltration and the increase in fibrotic area, and upregulated AMPK phosphorylation in the kidneys of HFD-fed mice; thus, it may ameliorate HFD-induced kidney injury.

中文翻译：

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木质素衍生的低分子量氧化木质素酚可刺激高脂饮食喂养小鼠的AMP活化蛋白激酶并抑制肾脏炎症和间质纤维化。

体重过多和肥胖会增加患上慢性肾脏病主要危险因素的风险。木质素占全球植物生物量的20％-30％；但是，由于其对化学和生物降解的抵抗力，因此不能很好地利用。我们调查了木质素衍生物低分子量氧化木质素酚（LOLP）是否可以改变高脂饮食（HFD）喂养小鼠肾脏的炎症和纤维化。将雄性小鼠分为三个治疗组：HFD； HFD；和HDF。HFD + 0.3％跌落 和HFD + 0.6％LOLP。对照小鼠（续）饲喂低脂饮食。检查了巨噬细胞动力学，纤维化程度，AMP激活的蛋白激酶（AMPK）的磷酸化程度以及肾脏促炎性介质的mRNA表达。巨噬细胞数量，纤维化面积百分比，HFD组小鼠肾脏中促炎性标志物TNF-α和Ccl2的mRNA表达以及纤维化标志物TGF-β的表达明显高于Cont组。相反，用0.6％LOLP治疗8周可显着抑制巨噬细胞浸润程度，间质纤维化区域以及HFD诱导的促炎和纤维化标记物的mRNA表达增加。总之，LOLP抑制了喂食HFD的小鼠肾脏中的巨噬细胞浸润和纤维化区域的增加，并上调了AMPK磷酸化。因此，它可以减轻HFD引起的肾脏损伤。6％的LOLP持续8周可显着抑制巨噬细胞浸润的程度，间质纤维化区域以及HFD诱导的促炎和纤维化标记物mRNA表达的增加。总之，LOLP抑制了喂食HFD的小鼠肾脏中的巨噬细胞浸润和纤维化区域的增加，并上调了AMPK磷酸化。因此，它可以减轻HFD引起的肾脏损伤。6％的LOLP持续8周可显着抑制巨噬细胞浸润的程度，间质纤维化区域以及HFD诱导的促炎和纤维化标记物mRNA表达的增加。总之，LOLP抑制了喂食HFD的小鼠肾脏中的巨噬细胞浸润和纤维化区域的增加，并上调了AMPK磷酸化。因此，它可以减轻HFD引起的肾脏损伤。