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TANG Huan-wen, HU Da-lin, LIANG Hai-rong, . Effects of nicotinamide on renal NF-κB expression in diabetic rats[J]. Chinese Journal of Public Health, 2008, 24(11): 1356-1358. DOI: 10.11847/zgggws2008-24-11-41
Citation: TANG Huan-wen, HU Da-lin, LIANG Hai-rong, . Effects of nicotinamide on renal NF-κB expression in diabetic rats[J]. Chinese Journal of Public Health, 2008, 24(11): 1356-1358. DOI: 10.11847/zgggws2008-24-11-41

Effects of nicotinamide on renal NF-κB expression in diabetic rats

  • Objective To study the expression of NF-κB in renal tissue of diabetic rat and its relationship with renal impairment,and to investigate the effect of nicotinamide on NF-κB in diabetic rat.Methods Thirty-six rats were randomly divided into control group,diabetic group and nicotinamide treatment group.The kidneys were taken out from all the rats to measure the NF-κB activity by electro phoretic mobility shift assays(EMSA),as well as to observe the glomerular basement membr ane(GBM)thickening and mesangial matrix(MM)density by electronic microscope.24 hour urine was collected to measure the levels of albumin(urine albumin excretion,UAE).The effects of nicotinamide on renal NF-κB expression in diabetic rats were studied by using immunocy tochemical techniques.The relatio nship between expression of NF-κB and ICAM-1,macrophage accumulation,renal function in diabetic rats were examined.Results The expression of NF-κB in diabetic rat was higher than that of normal control(P<0.01).The number of positive cells expressing NF-κB(9.18±2.42)in glomerulus of diabetic rats showed a strong correlation with ICAM-1 expression(0.3973±0.0312),macrophage accumulation(8.14±3.43)with the correlation coefficients of 0.57 and 0.68,respectively.Nicotinamide significantly inhibited the expression of NF-κB,reduced the GBM thickening(337.1±67.9 nm) and the MM density(39.58±6.21μm2/μm2) (P <0.01).The renalfunction and the renaltissue injury were improved.Conclusion The renal protection of nicotinamide is partly associated with the inhibit on of NF-κB activation,down-regulating of ICAM-1 expression and macrophage infiltration in diabetic nephropathy model.
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