期刊
FOOD & FUNCTION
卷 8, 期 7, 页码 2536-2547出版社
ROYAL SOC CHEMISTRY
DOI: 10.1039/c7fo00490g
关键词
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资金
- National Natural Science Foundation of China [C31671823]
- Excellent Doctoral Dissertation Funded Projects of Shaanxi Normal University, China [X2014YB09]
- Fundamental Research Funds for the Central Universities of Shaanxi Normal University, China [GK201604012]
- Development program for Innovative Research Team of Shaanxi Normal University, China [GK201501006]
- Construction Program of Chongqing Collaborative Innovation Center for Functional Food
- Chongqing University of Education [167001]
- Science and Technology Innovation as a Whole Plan Projects of Shaanxi Province, China [2015KTCQ02-01]
The present study was designed to investigate the protective effects of Ilex Kuding tea polysaccharides (IKTP) on high fructose (HF)-induced liver injury and vascular endothelial dysfunction in mice. IKTP were identified as acidic heteropolysaccharides by FT-IR and HPLC. Healthy male Kunming mice fed 20% fructose in drinking water for 8 consecutive weeks significantly displayed dyslipidemia, hepatic steatosis, oxidative stress and vascular endothelial dysfunction. However, continuous administration of IKTP at 200, 400 and 800 mg per kg bw in HF-fed mice could prevent the damage caused by HF-diets, especially at dosages of 400 and 800 mg per kg bw (p < 0.01). IKTP significantly reduced the HF-induced elevation of the serum TC, TG, LDL-C, TXA(2) and ET-1 levels, as well as AST and ALT activities, while markedly increased the HF-induced decline of HDL-C, PGI(2) and eNOS levels in the serum compared to HF-fed mice. Meanwhile, the hepatic MDA level was lowered while SOD and GSH-Px activities were increased in IKTP-treated mice, compared to HF-fed mice. Histopathology of the liver and cardiovascular aortic by H&E or oil red O staining confirmed the liver steatosis and the vascular injury induced by HF-diets and the protective effects of IKTP. These findings suggest that HF causes oxidative damage, and IKTP alleviates liver injury and vascular endothelial dysfunction.
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