4.7 Article

Protective effects of allicin on streptozotocin-induced diabetic nephropathy in rats

Journal

JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE
Volume 97, Issue 4, Pages 1359-1366

Publisher

WILEY
DOI: 10.1002/jsfa.7874

Keywords

allicin; diabetic nephropathy; transforming growth factor beta 1; phosphorylated extracellular signal-regulated kinase 1/2

Funding

  1. Natural Science Foundation of Zhejiang Province, China [Y2110918]
  2. Chinese Traditional Medicine Science and Technology Plan of Zhejiang province, China [2011ZA008]

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BACKGROUND: Studies in animal models have shown that allicin, a major biologically active component of garlic, can play a role in the prevention of tissue fibrosis in the liver, lung and heart, mainly related to the inhibition of fibroblast proliferation, fibrogenic cytokine secretion and extracellular matrix synthesis. This study aimed to investigate the protective effects of allicin on renal damage in streptozotocin (STZ)-induced diabetic rats. STZ-induced diabetic rats were administered allicin (15, 30 and 45mg kg(-1) day(-1)) via daily intra-gastric gavage for 12 weeks. The levels of fasting blood glucose (FBG), blood urea nitrogen (BUN), serum creatinine (sCr), lipid and 24 h urine albumin excretion (UAE) were measured at the end of weeks 4, 8 and 12. The renal histopathology and the expression levels of collagen I, transforming growth factor.. 1 (TGF-beta 1) and phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) were measured using immunohistochemistry and/or western blotting. RESULTS: In 12 week STZ-induced diabetic rats, severe hyperglycemia and albuminuria were markedly developed. Treatment with allicin for 12 weeks ameliorated diabetes-induced morphological alterations of the kidney and decreased FBG, BUN, sCr, triglyceride (TG) and 24 h UAE in diabetic rats. The expression levels of collagen I, TGF-beta 1 and p-ERK1/2 were significantly decreased by allicin treatment. CONCLUSION: These results suggested that allicin may play a protective role in diabetic nephropathy via the TGF-beta 1/ERK pathway in diabetic rats. (C) 2016 Society of Chemical Industry

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