Chronic inhibition of nuclear factor kappa B attenuates aldosterone/salt-induced renal injury

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• 作者：Wei Ding ; Lei Yang ; Minmin Zhang ; ^{zhangminmin03@yahoo.com.cn} ; Yong Gu
• 关键词：Aldosterone ; Nuclear factor kappa B ; Inflammation ; Chronic kidney disease
• 刊名：Life Sciences
• 出版年：2012
• 期刊代码：62_00243205
• 类别：imm
• 出版时间：20 April, 2012
• 卷：90
• 期：15-16
• 页码：600-606
• 文件大小：1119 K

摘要

Aims

Recent studies suggested that nuclear factor kappa B (NF-魏B) plays a key role in the pathogenesis of renal injury. This study investigated whether NF-魏B inhibition attenuates progressive renal damage in aldosterone/salt-induced renal injury and its mechanisms.

Main methods

Adult male rats were uninephrectomized and treated with one of the following for 4 weeks: vehicle (0.5%ethanol, subcutaneously); vehicle/1%NaCl (1%NaCl in drinking solution); aldosterone/1%NaCl (1%NaCl in drinking solution and aldosterone, 0.75 渭g/h, subcutaneously); or aldosterone/1%NaCl + pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-魏B (100 mg/kg/day, by gavage). The activity of NF-魏B was measured by EMSA and immunohistochemistry, CTGF and ICAM-1 were measured by Western blot and real-time PCR, and TGF-尾 and CTGF were measured by immunohistochemistry.

Key findings

Rats that received aldosterone/1%NaCl exhibited hypertension and severe renal injury. Renal cortical mRNA levels of CTGF, TGF-尾, ICAM-1 and collagen IV, protein expression of CTGF and ICAM-1, and NF-魏B-DNA binding activity were significantly upregulated in rats that received aldosterone/1%NaCl. Treatment with PDTC significantly decreased the percentage of cells positive for CTGF and TGF-尾; mRNA levels of CTGF, TGF-尾, ICAM-1 and collagen IV, and protein levels of CTGF and ICAM-1 were also inhibited by PDTC.

Significance

These data suggest that the NF-魏B signal pathway plays a role in the progression of aldosterone/salt-induced renal injury.