Protective effect of Lycium barbarum polysaccharides against high-fat diet-induced renal injury and lipid deposition in rat kidneys

J. Liao, B. Liu, W. Zhong, G-D. Wang, Y-L. Xu, X. Chen

Article ID: 4540
Vol 33, Issue 1, 2019
DOI: https://doi.org/10.54517/jbrha4540
Received: 4 June 2018; Accepted: 4 June 2018; Available online: 11 March 2019; Issue release: 11 March 2019

Abstract

This study aimed to explore the protective effect of Lycium barbarum polysaccharides (LBPs) against hyperlipidemia and lipid-induced renal injury in a rat model. Male Sprague-Dawley rats (n=30) were randomly divided into three equal groups: a control group (fed a regular diet) and two experimental groups (fed a high-fat diet). By feeding rats a high-fat diet for 12 weeks, an animal model of hyperlipidemia was established, after which one experimental group received oral LBPs at a dose of 300 mg/kg per day. Blood lipids, renal function, and urinary proteins were measured after 12 weeks. Changes in renal pathology and expression levels of sterol regulatory element binding transcription factor 1 (SREBP-1), interleukin-6 (IL- 6), tumor necrosis factor-alpha (TNF-α), AMP-activated protein kinase (AMPK) were determined. Rats with hyperlipidemia induced by a high-fat diet showed increases in blood lipids and blood urea nitrogen, serum creatinine, and urinary protein, as well as increases in renal levels of SREBP-1, TNF-α, and IL-6 and decreases in renal levels of adiponectin and AMPK. Administration of LBPs restored blood lipid, blood urea nitrogen, serum creatinine, and urinary protein levels, downregulated renal levels of SREBP-1, TNF-α, and IL-6, and upregulated renal levels of adiponectin and AMPK. These results indicate that LBPs may mediate lipid metabolism, enhance anti-inflammatory responses, and ameliorate renal injury caused by lipid metabolism isorders in a rat model of hyperlipidemia.


Keywords

hyperlipidemia;lipid metabolism;lipid-induced kidney injury


References

Supporting Agencies



Copyright (c) 2019 J. Liao, B. Liu, W. Zhong, G-D. Wang, Y-L. Xu, X. Chen




This site is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).