Effect of bone morphogenetic protein 4 on the infiltration of macrophages and the expression of nuclear factor-κB in mice model of unilateral ureteral obstruction
10.3760/cma.j.issn.1673-4912.2017.10.004
- VernacularTitle:骨形成蛋白4对单侧输尿管梗阻小鼠肾间质巨噬细胞聚集及核因子-κB信号通路的影响
- Author:
Qiang FU
1
;
Ting WANG
;
Huina YU
;
Konggui YU
;
Linfei TANG
;
Qihua FENG
Author Information
1. 434020,荆州市中心医院儿科
- Keywords:
Bone morphogenetic protein 4;
Ureteral obstruction;
unilateral;
Macrophage;
Nuclear factor-κB
- From:
Chinese Pediatric Emergency Medicine
2017;24(10):733-736
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of bone morphogenetic protein 4(BMP4) on the infil-tration of macrophages and the expression of nuclear factor-κB in mice model of unilateral ureteral obstruc-tion(UUO).Methods C57BL/6 mice were randomly divided into four groups:injected intra-abdominally with saline-sham-operated group(saline-sham group,n =8),injection intra-abdominally with saline-UUO-operated group(saline-UUO group,n=8),injection intra-abdominally with anti-BMP4-sham-operated group (anti-BMP4-sham group,n=8),and injection intra-abdominally with anti-BMP4-UUO-operated group(anti-BMP4-UUO group,n=8).Either saline or anti-BMP4(group 200 μl/gram of body weight per day) were injected intra-abdominally for 7 days after surgery.Mice were sacrificed at 7th day to evaluate the expression of CD68 and p-P65 by immunohistochemical staining in each group.Besides,the p-P65 protein level was also analyzed by Western blotting in four groups.Results Immunohistochemical staining showed that the expres-sions of CD68 and p-P65 were significantly reduced in the kidney cortices in anti-BMP4-UUO group than in saline-UUO group(P<0.05,respectively).Similar to that,the p-P65 protein level was significantly reduced in the kidney cortices in anti-BMP4-UUO group than in saline-UUO group(P < 0.05,respectively). Conclusion BMP4 participates in the process of renal interstitial inflammation in obstructive nephropathy, and may play a role through the activation of nuclear factor-κB signaling pathway.
