2007Zhongguo tangniaobing zazhiRequires access

Effect of atorvastatin on NF-κB in peripheral blood mononuclear cells and renal tissues in diabetic rats

Li Lon

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Abstract

Objective To investigate the protective effect of atorvastatin on diabetic nephropathy(DN)and its mechanisms.Methods The rat diabetic model was made by the intra-peritoneal injection of streptozocin.The rats were divided into three groups of normal control,diabetes,diabetes treated with atorvastatin(2 mg·kg-1·d-1)by gavage.Activity of nuclear factor kappa B(NF-κB)in peripheral blood mononuclear cells(PBMC)was analyzed by Enzyme-linked Immunosorbent Assay(ELISA).Expressions of NF-κB,MCP-1 and fibronectin(FN)in renal tissue were measured by immunohisto-chemical stain,24-hour urinary protein,and plasma creatinine(Cr)were measured.Results NF-κB activities in PBMC and renal tissues(RT)in diabetic rats were significantly higher than those in normal rats(2.45±0.31 vs 0.37±0.15,as OD value in PBMC P0.01;9.842±1.653 vs 1.116±0.467 as NF-κB positive cell number in RT,P0.01).While compared with diabetic rats,atorvastatin treatment significantly inhibited activation of NF-κB(0.58±0.06 vs 2.45±0.31,P0.05 in PBMC;4.158±1.552 vs 9.842±1.653,P0.05 in RT),reduced expression of FN,decreased urine protein excretion,ameliorated mononuclear infiltration,improved renal function and pathological changes of renal histology.Conclusions These results suggest the activated NF-κB plays a pathogenic role for diabetic nephropathy.Atorvastatin treatment slows down the development of DN.The protective effect of atorvastatin on DN appears to be mediated through the inhibition of activation of NF-κB.

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Objective To investigate the protective effect of atorvastatin on diabetic nephropathy(DN)and its mechanisms.Methods The rat diabetic model was made by the intra-peritoneal injection of streptozocin.The rats were divided into three groups of normal control,diabetes,diabetes treated with atorvastatin(2 mg·kg-1·d-1)by gavage.Activity of nuclear factor kappa B(NF-κB)in peripheral blood mononuclear cells(PBMC)was analyzed by Enzyme-linked Immunosorbent Assay(ELISA).Expressions of NF-κB,MCP-1 and fibronectin(FN)in renal tissue were measured by immunohisto-chemical stain,24-hour urinary protein,and plasma creatinine(Cr)were measured.Results NF-κB activities in PBMC and renal tissues(RT)in diabetic rats were significantly higher than those in normal rats(2.45±0.31 vs 0.37±0.15,as OD value in PBMC P0.01;9.842±1.653 vs 1.116±0.467 as NF-κB positive cell number in RT,P0.01).While compared with diabetic rats,atorvastatin treatment significantly inhibited activation of NF-κB(0.58±0.06 vs 2.45±0.31,P0.05 in PBMC;4.158±1.552 vs 9.842±1.653,P0.05 in RT),reduced expression of FN,decreased urine protein excretion,ameliorated mononuclear infiltration,improved renal function and pathological changes of renal histology.Conclusions These results suggest the activated NF-κB plays a pathogenic role for diabetic nephropathy.Atorvastatin treatment slows down the development of DN.The protective effect of atorvastatin on DN appears to be mediated through the inhibition of activation of NF-κB.

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Available abstract

Objective To investigate the protective effect of atorvastatin on diabetic nephropathy(DN)and its mechanisms.Methods The rat diabetic model was made by the intra-peritoneal injection of streptozocin.The rats were divided into three groups of normal control,diabetes,diabetes treated with atorvastatin(2 mg·kg-1·d-1)by gavage.Activity of nuclear factor kappa B(NF-κB)in peripheral blood mononuclear cells(PBMC)was analyzed by Enzyme-linked Immunosorbent Assay(ELISA).Expressions of NF-κB,MCP-1 and fibronectin(FN)in renal tissue were measured by immunohisto-chemical stain,24-hour urinary protein,and plasma creatinine(Cr)were measured.Results NF-κB activities in PBMC and renal tissues(RT)in diabetic rats were significantly higher than those in normal rats(2.45±0.31 vs 0.37±0.15,as OD value in PBMC P0.01;9.842±1.653 vs 1.116±0.467 as NF-κB positive cell number in RT,P0.01).While compared with diabetic rats,atorvastatin treatment significantly inhibited activation of NF-κB(0.58±0.06 vs 2.45±0.31,P0.05 in PBMC;4.158±1.552 vs 9.842±1.653,P0.05 in RT),reduced expression of FN,decreased urine protein excretion,ameliorated mononuclear infiltration,improved renal function and pathological changes of renal histology.Conclusions These results suggest the activated NF-κB plays a pathogenic role for diabetic nephropathy.Atorvastatin treatment slows down the development of DN.The protective effect of atorvastatin on DN appears to be mediated through the inhibition of activation of NF-κB.

Key concepts: Diabetic nephropathy, Peripheral blood mononuclear cell, Atorvastatin, Internal medicine, Endocrinology, Diabetes mellitus, Medicine, Mononuclear cell infiltration

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