2005Zhonghua neifenmi daixie zazhiRequires access

Inhibitory effects of rosiglitazone on activation of NF-κB and expression of MCP-1 induced by high glucose in rat mesangial cells

Lin Peng

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Abstract

The rat mesangial cells (MCs) were cultured in the medium with normal glucose (5.6 mmol/L,NG), high glucose (25 mmol/L, HG), HG+5 μmol/L Rosiglitazone, HG+20 μmol/L Rosiglitazone and HG+PDTC (a NF-κB inhibitor). The results showed that HG increased MCP-1 mRNA expression by 2.94-fold at 24 h, which was prevented by Rosiglitazone (20 μmol/L) pretreatment. The NF-κB binding activity was 2.5-fold higher in MCs exposed to HG than normal glucose .When the MCs were cultured in the presence of Rosiglitazone (20 μmol/L) for 1 h, there was a highly significant reduction in NF-κB binding activity . This study suggests that Rosiglitazone may inhibit high glucose-induced NF-κB activation and MCP-1 expression in mesangial cells.These findings may provide an experimental evidence for further evaluating the possible protective effect of Rosiglitazone against diabetic nephropathy.

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What this paper is about

The rat mesangial cells (MCs) were cultured in the medium with normal glucose (5.6 mmol/L,NG), high glucose (25 mmol/L, HG), HG+5 μmol/L Rosiglitazone, HG+20 μmol/L Rosiglitazone and HG+PDTC (a NF-κB inhibitor). The results showed that HG increased MCP-1 mRNA expression by 2.94-fold at 24 h, which was prevented by Rosiglitazone (20 μmol/L) pretreatment. The NF-κB binding activity was 2.5-fold higher in MCs exposed to HG than normal glucose .When the MCs were cultured in the presence of Rosiglitazone (20 μmol/L) for 1 h, there was a highly significant reduction in NF-κB binding activity . This study suggests that Rosiglitazone may inhibit high glucose-induced NF-κB activation and MCP-1 expression in mesangial cells.These findings may provide an experimental evidence for further evaluating the possible protective effect of Rosiglitazone against diabetic nephropathy.

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Available abstract

The rat mesangial cells (MCs) were cultured in the medium with normal glucose (5.6 mmol/L,NG), high glucose (25 mmol/L, HG), HG+5 μmol/L Rosiglitazone, HG+20 μmol/L Rosiglitazone and HG+PDTC (a NF-κB inhibitor). The results showed that HG increased MCP-1 mRNA expression by 2.94-fold at 24 h, which was prevented by Rosiglitazone (20 μmol/L) pretreatment. The NF-κB binding activity was 2.5-fold higher in MCs exposed to HG than normal glucose .When the MCs were cultured in the presence of Rosiglitazone (20 μmol/L) for 1 h, there was a highly significant reduction in NF-κB binding activity . This study suggests that Rosiglitazone may inhibit high glucose-induced NF-κB activation and MCP-1 expression in mesangial cells.These findings may provide an experimental evidence for further evaluating the possible protective effect of Rosiglitazone against diabetic nephropathy.

Key concepts: Rosiglitazone, Endocrinology, Internal medicine, Diabetic nephropathy, Chemistry, NF-κB, Diabetes mellitus, Medicine

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