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Nuclear Factor 魏B-Dependent Anti-inflammatory Effects of s-Allyl Cysteine and s-Propyl Cysteine in Kidney of Diabetic Mice
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  • 作者:Mei-chin Mong ; Mei-chin Yin
  • 刊名:Journal of Agricultural and Food Chemistry
  • 出版年:2012
  • 出版时间:March 28, 2012
  • 年:2012
  • 卷:60
  • 期:12
  • 页码:3158-3165
  • 全文大小:321K
  • 年卷期:v.60,no.12(March 28, 2012)
  • ISSN:1520-5118
文摘
Renal protection of s-allyl cysteine (SAC) and s-propyl cysteine (SPC) in diabetic mice against inflammatory injury was examined. Each agent at 0.5 and 1 g/L was added to the drinking water for 10 weeks. SAC or SPC intake significantly reduced the plasma blood urea nitrogen level and increased creatinine clearance (P < 0.05). These treatments significantly lowered the renal level of reactive oxygen species, nitric oxide, interleukin-6, tumor necrosis factor-伪, and prostaglandin E2 in diabetic mice (P < 0.05). Renal mRNA expression of inducible nitric oxide synthase, cyclooxygenase-2, protein kinase C (PKC)-伪, PKC-尾, and PKC-纬 was enhanced in diabetic mice (P < 0.05); however, SAC or SPC treatments dose dependently declined mRNA expression of these factors (P < 0.05). Nuclear factor 魏B (NF-魏B) activity, mRNA expression, and protein production in kidney of diabetic mice were significantly increased (P < 0.05). SAC or SPC intake dose dependently suppressed NF-魏B activity, NF-魏B p65 mRNA expression, and protein level (P < 0.05). Diabetes also enhanced renal protein expression of mitogen-activated protein kinase (P < 0.05). SAC and SPC, only at a high dose, significantly suppressed protein production of p-p38 and p-ERK1/2 (P < 0.05). Renal mRNA expression and protein generation of peroxisome proliferator-activated receptor (PPAR)-伪 and PPAR-纬 were significantly down-regulated in diabetic mice (P < 0.05), but the intake of SAC or SPC at high dose up-regulated PPAR-伪 and PPAR-纬 (P < 0.05). These findings support that SAC and SPC are potent anti-inflammatory agents against diabetic kidney diseases.

Keywords:

s-allyl cysteine; s-propyl cysteine; diabetes; NF-魏B; MAPK; PPAR

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