4.7 Article

The renal protective effects of Anoectochilus roxburghii polysaccharose on diabetic mice induced by high-fat diet and streptozotocin

期刊

JOURNAL OF ETHNOPHARMACOLOGY
卷 178, 期 -, 页码 58-65

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2015.12.002

关键词

Anoectochilus roxburghii; Polysaccharose; Diabetic renal damage; p38 MAP kinase; Inflammation

资金

  1. National Natural Science Foundation of China [20972061]
  2. Fujian Province Natural Science Foundation of China [2013J01337]

向作者/读者索取更多资源

Ethnopharmacological relevance: Anoectochilus roxburghii (Wall.) Lindl. 1832 is an herbal medicine used to treat diabetes in China. Considering that Anoectochilus roxburghii polysaccharose (ARP) is the main constituent of Anoectochilus roxburghii, the present study is aimed to investigate the renal protection of ARP and its possible mechanism in diabetic mice. Materials and methods: Institute of Cancer Research (ICR) mice were induced to diabetes with high-fat diet (HFD) and low-dose streptozotocin (STZ). ARP (100, 300 mg/kg) was orally administrated to diabetic mice once a day for consecutive 15 days. The fasting glucose level, expressions of key proteins of p38 MAP kinase cascade, inflammatory factors, fibronectin (FN) and the activities of matrix metalloproteinases (MMPs) were measured. Furthermore, the histological examination of the separated kidneys was also carried out. Results: Compared with the diabetic mice, ARP administration induced a significant decrease in blood glucose level and improved the body weight of diabetic mice. In addition, ARP inhibited the expression of renal p38 MAP kinase cascade and its downstream inflammatory factors including tumor necrosis factor alpha (TNF-alpha), monocyte chemoattractant protein-1 (MCP-1), FN as well as MMP2/9. Moreover, the histological examination showed an apparent reduction of mesangial matrix deposition and damage of microvascular structure after ARP administration. Conclusions: The protective effects of ARP on diabetic renal damage may be attributed to the inhibition of p38 MAP kinase cascade and then attenuating the inflammatory responses and high glucose-induced renal damage. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

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