查看文章

Inflammatory cell infiltration plays a key role in the onset and progression of renal injury. The NF-κB participates in the inflammatory response, regulating many proinflammatory genes. Angiotensin II (Ang II), via AT 1 and AT 2 receptors, activates NF-κB. Although the contribution of Ang II to kidney damage progression is already established, the receptor subtype involved in the inflammatory cell recruitment is not clear. For investigating this issue, the unilateral ureteral obstruction (UUO) model was used in mice, blocking Ang II production/receptors and NF-κB pathway. Two days after UUO, obstructed kidneys of wild-type mice presented a marked interstitial inflammatory cell infiltration and increased NF-κB activity. Treatment with AT 1 or AT 2 antagonists partially decreased NF-κB activation, whereas only the AT 2 blockade diminished monocyte infiltration. Obstructed kidneys of AT 1-knockout mice showed interstitial …