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Mangiferin Attenuates Renal Fibrosis Through Down‐Regulation of Osteopontin in Diabetic Rats
Author(s) -
Zhu Xia,
Cheng YaQin,
Du Lei,
Li Yu,
Zhang Fan,
Guo Hao,
Liu YaoWu,
Yin XiaoXing
Publication year - 2015
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.5254
Subject(s) - mangiferin , osteopontin , medicine , kidney , endocrinology , streptozotocin , fibrosis , inflammation , diabetic nephropathy , diabetes mellitus , pharmacology
This study was designed to investigate the effects of mangiferin on renal fibrosis, osteopontin production, and inflammation in the kidney of diabetic rats. Diabetes was induced through the single administration of streptozotocin (55 mg/kg, i.p.). Diabetic rats were treated with mangiferin (15, 30, and 60 mg/kg/day, i.g.) for 9 weeks. The kidney was fixed in 10% formalin for glomerulus fibrosis examination using Masson trichrome staining. Kidney and blood were obtained for assays of the associated biochemical parameters. Chronic mangiferin treatment prevented renal glomerulus fibrosis evidenced by decreases in Mason‐stained positive area of glomeruli, protein expression of type IV collagen, and α‐smooth muscle actin in the kidney of diabetic rats, in comparison with decreases in mRNA and protein expression of osteopontin as well as protein expression of cyclooxygenase 2 and NF‐кB p65 subunit in the renal cortex of diabetic rats. Moreover, mangiferin reduced the levels of interleukin 1β in both the serum and the kidney of diabetic rats. Our findings demonstrate that mangiferin prevents the renal glomerulus fibrosis of diabetic rats, which is realized through the suppression of osteopontin overproduction and inflammation likely via inactivation of NF‐кB. Copyright © 2014 John Wiley & Sons, Ltd.