Myrciaria cauliflora extract improves diabetic nephropathy via suppression of oxidative stress and inflammation in streptozotocin-nicotinamide mice

被引:47
作者
Hsu, Jeng-Dong [1 ,2 ]
Wu, Chia-Chun [3 ]
Hung, Chi-Nan [4 ]
Wang, Chau-Jong [5 ,6 ]
Huang, Hui-Pei [5 ,6 ,7 ]
机构
[1] Chung Shan Med Univ, Dept Pathol, Taichung, Taiwan
[2] Chung Shan Med Univ Hosp, Taichung, Taiwan
[3] Chi Mei Med Ctr, Div Nephrol, Dept Internal Med, Tainan, Taiwan
[4] Ming Dao Univ, Dept Holist Wellness, Changhua, Taiwan
[5] Chung Shan Med Univ, Inst Biochem & Biotechnol, 110,Sect 1,Jianguo North Rd, Taichung, Taiwan
[6] Chung Shan Med Univ Hosp, Clin Lab, Taichung, Taiwan
[7] Chung Shan Med Univ, Sch Med, Dept Biochem, 110,Sect 1,Jianguo North Rd, Taichung, Taiwan
关键词
diabetic nephropathy; inflammation; Myrciaria cauliflora extract (MCE); oxidative stress; CORCHORUS-OLITORIUS LEAVES; ACTIVATED PROTEIN-KINASE; HIGH-FAT DIET; AMELIORATES HYPERGLYCEMIA; INSULIN SENSITIVITY; SIGNALING PATHWAY; KIDNEY-DISEASE; RENAL-DISEASE; C ISOFORMS; KAPPA-B;
D O I
10.1016/j.jfda.2016.03.009
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Myrciaria cauliflora is a functional food rich in anthocyanins, possessing antioxidative and anti-inflammatory properties. Our previous results demonstrated M. cauliflora extract (MCE) had beneficial effects in diabetic nephropathy (DN) and via the inhibition of Ras/ PI3K/Akt and kidney fibrosis-related proteins. The purpose of this study was to assess the benefit of MCE in diabetes associated with kidney inflammation and glycemic regulation in streptozotocin nicotinamide (STZ/NA)-induced diabetic mice. Compared with the untreated diabetic group, MCE significantly improved blood glucose and serum biochemical characteristic levels. Exposure to MCE increased antioxidative enzyme activity and diminished reactive oxygen synthesis. Mice receiving MCE supplementation had reduced intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), monocyte chemoattractant protein 1 (MCP-1), colony stimulating factor 1 (CSF-1), interleukin-1 beta (IL-1 beta), IL-6 and tumor necrosis factor alpha (TNF-alpha) levels compared to the untreated diabetic mice. Inflammatory and fibrotic related proteins such as collagen IV, fibronectin, Janus kinase (JAK), phosphorylated signal transducer and activator of transcription 3 (STAT3), protein kinase C beta (PKC-beta), and nuclear factor kappa B (NF-kappa B) were also inhibited by MCE treatment in STZ/NA mice. These results suggest that MCE may be used as a hypoglycemic agent and antioxidant in Type 2 diabetic mice. Copyright (C) 2016, Food and Drug Administration, Taiwan. Published by Elsevier Taiwan LLC.
引用
收藏
页码:730 / 737
页数:8
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