中文摘要：

为了在到 tubulointerstitial 纤维变性的老鼠残余肾和它的贡献观察树枝状的房间(DC ) 的累积，在 DC 上的 valsartan 的影响下面，一个老鼠残余肾模型被小计肾切除术建立。四个试验性的组被包括：正常，假冒，模型(SNx ) 和这个组与 Valsartan (SNxV ) 对待。老鼠分别地在星期 1,4 和 12 点被打死。CD1a+CD80+ DC 是由两倍 immunostaining 方法的 assayed，图象与 Axioplan 2 显微镜学被分析。P-selectin， TGF-1， -SMA, 骨胶原和 fibronectin 的表情被 immunohistochemistry 或 semiquantitative RT-PCR 分析，并且 tubulointerstitial firosis (TIF ) 的水平被获得。CD1a+CD80+ DC 逐渐地在肾的小管， interstitium 和容器之中被增加，特别在在在星期 12 点的模型组的 DC 的 interstitium，和数字在在星期 1 或 4 点的模型组是多于那的大部分。在 tubulointerstitial 区域和 TIF 的度的 P-selectin， TGF-1， -SMA, 骨胶原和 fibronectin 的表情在星期 12 点在模型组实质地被增加。在 interstitium 的 DC 的累积很好与肾的功能和 tubulointerstitial 纤维变性的前进的损失被联系。Valsartan 处理禁止了 DC 的本地累积并且稀释了肾的 tubulointerstitial 损坏。本地 DC 累积与跟随肾的脱离的 tubulointerstitial 纤维变性和肾的机能障碍有关。对血管收缩素的封锁可能是稀释肾的免疫煽动性的损害的一个有势力方法。

英文摘要：

To observe the accumulation of dendritic cells （DCs） in rat remnant kidney and its contribution to tubulointerstitial fibrosis, under influence of valsartan on DCs, a rat remnant kidney model was established by subtotal nephrectomy. Four experimental groups were included： normal, sham, model （SNx） and the group treated with Valsartan （SNxV）. Rats were killed at week 1, 4 and 12, respectively. CD1a^＋CD80^＋ DCs were assayed by double immunostaining method and the images were analyzed with Axioplan 2 microscopy. The expressions of P-selectin, TGF-β1, α-SMA, collagen Ⅲ and fibronectin were analyzed by immunohistochemistry or semi- quantitative RT-PCR, and the level of tubulointerstitial firosis （TIF） was scored. CD1a^＋CD80^＋ DCs were gradually increased among renal tubules, interstitium and vessels, especially in interstitium, and the number of DCs in model group at week 12 was much more than that in model groups at week 1 or 4. The expressions of P-selectin, TGF-β1, α-SMA, collagen Ⅲ and fibronectin in tubulointerstitial areas and the degree of TIF were increased substantially in model group at week 12. The accumulation of DCs in interstitium was well associated with the loss of renal function and the progression of tubulointerstitial fbrosis. Valsartan treatment inhibited the local accumulation of DCs and attenuated renal tubulointerstitial damage. The local DCs accumulation was related to tubulointerstitial fibrosis and renal dysfunction following renal ablation. Blockade to angiotensin II might be a potent way to attenuate renal immuno-inflammatory injury. Cellular ＆ Molecular Immunology. 2006;3（3）：213-220.