In this study, a diabetic kidney disease model was established by placing the test rats on a high-sugar/high-fat diet combined with streptozotocin induction. Histopathological examination (H&E, Masson, and PASM stain) showed pathological changes in the diabetic rat kidneys, in addition to fibrotic symptoms and collagen deposition. Immunohistochemistry and western blot analyses indicated that the diabetic condition significantly increased the expressions of fibrotic markers including collagen, α-SMA, and fibronectin. The levels of cholesterol, triglyceride, and low-density lipoprotein were also increased in diabetic kidney disease (DKD) rat blood, while the level of high-density lipoprotein was decreased. The results of Oil red O staining experiments indicated that the kidneys of diabetic rats exhibited appreciable fat deposition, with high contents of triglyceride and cholesterol. To inhibit fibrosis and reduce fat deposition, low molecular weight fucoidan (LMWF) may be used. Based on PCR and western blot analyses, LMWF can regulate the expression levels of important lipid metabolism regulators, thereby impeding the development of kidney fibrosis. Through the vitro model, it also be indicated that LMWF could inhibit fibrosis process through regulating lipid metabolism which induced by palmitic acid.

In this study, sulfated polysaccharides extracted from Laminaria japonica were degraded by free radicals to obtain low–molecular weight fucoidan (LMWF). The effects of LMWF on bleomycin-treated pulmonary fibrosis (PF) mice were evaluated in precious research. In this study, the expression of M2 macrophage polarization biomarker arginase was detected by immunohistochemistry, and the expression of M1/M2 markers was detected by Western blot and qPCR. It was found that the expression of M1/M2 macrophage markers were significantly increased in the lung tissue of pulmonary fibrosis mice, and LMWF could effectively reduce its expression. Subsequently, in order to verify the mechanism of LMWF inhibiting pulmonary fibrosis by regulating macrophage polarization, MH-S cells were induced by LPS combined with IFN-γ and IL-4 to construct the in vitro macrophage polarization models, and the expression of biomarkers were analyzed by Western blot and qPCR. The results showed that LMWF could regulate M1 macrophage polarization through early anti-inflammatory effect and inhibit the development of pulmonary fibrosis by inhibiting M2 macrophage polarization in the later stage.