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Low Molecular Weight Fucoidan Can Inhibit the Fibrosis of Diabetic Kidneys by Regulating the Kidney Lipid Metabolism
Yan Wang1, Yanlei Sun2, Fengli Shao3
1College of Pharmacy, Linyi University, Linyi, Shandong, China.
Abstract:
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.
Insights
Low molecular weight fucoidan (LMWF) effectively combats diabetic kidney disease (DKD) by reducing kidney fibrosis and fat deposition. It regulates lipid metabolism, offering a potential therapeutic strategy for DKD.
Area of Science:
- Nephrology
- Biochemistry
- Pharmacology
Background:
- Diabetic kidney disease (DKD) is characterized by kidney fibrosis and altered lipid metabolism.
- High-sugar/high-fat diets and streptozotocin induction are common methods for establishing DKD models in rats.
- Fibrotic markers like collagen, α-SMA, and fibronectin are elevated in DKD kidneys.
Purpose of the Study:
- To investigate the effects of low molecular weight fucoidan (LMWF) on kidney fibrosis and lipid metabolism in a rat model of DKD.
- To explore the potential of LMWF as a therapeutic agent for inhibiting fibrosis and reducing fat deposition in DKD.
Main Methods:
- Establishment of a DKD rat model using a high-sugar/high-fat diet and streptozotocin.
- Histopathological examinations (H&E, Masson, PASM staining) and immunohistochemistry.
- Western blot analysis for fibrotic markers and lipid metabolism regulators.
- Biochemical analysis of blood lipid profiles (cholesterol, triglycerides, HDL, LDL).
- Oil red O staining for kidney fat deposition.
- In vitro studies using palmitic acid-induced fibrosis.
Main Results:
- DKD rats exhibited significant kidney pathological changes, fibrosis, and collagen deposition.
- Expressions of fibrotic markers (collagen, α-SMA, fibronectin) were significantly increased in DKD kidneys.
- DKD rats showed dyslipidemia, with increased cholesterol, triglycerides, LDL, and decreased HDL.
- Kidneys of DKD rats displayed substantial fat deposition.
- LMWF treatment regulated lipid metabolism regulators and inhibited kidney fibrosis.
- LMWF demonstrated antifibrotic effects in vitro by modulating lipid metabolism.
Conclusions:
- LMWF effectively ameliorates kidney fibrosis and fat deposition in a rat model of DKD.
- LMWF exerts its therapeutic effects by regulating lipid metabolism and its associated fibrotic pathways.
- LMWF shows promise as a therapeutic agent for managing diabetic kidney disease.
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