Valsartan Inhibited the Accumulation of Dendritic Cells in Rat Fibrotic Renal Tissue  

作　　者：Kaiyin Wu Tong Zhou Guizhi Sun Weiming Wang Yumei Zhang Yanyun Zhang Li Hao Nan Chen 

机构地区：[1]Department of Nephrology, Rui Jin Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200025, China [2]Joint Immunology Laboratory, Institutes of Health Sciences and Shanghai Institute of Immunology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China

出　　处：《Cellular & Molecular Immunology》2006年第3期213-220,共8页中国免疫学杂志（英文版）

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.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.

关 键 词：dendritic cell tubulointerstitial fibrosis NEPHRECTOMY VALSARTAN 

分 类 号：R692[医药卫生—泌尿科学]