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目的 研究单侧输尿管梗阻后肾间质纤维化发生机理及血管紧张素转换酶抑制剂依那普利对其的调节作用。方法采用单侧输尿管结扎模型，造模５ｄ后用免疫组织化学法观察梗阻肾间质Ⅰ、Ⅲ、Ⅳ型胶原，α－平滑肌肌动蛋白（α－ＳＭＡ）的表达，Ｔ淋巴细胞浸润数；用逆转录聚合酶链反应（ＲＴ－ＰＣＲ）法观察梗阻肾组织转化生长因子β１（ＴＧＦ－β１）ｍＲＮＡ、组织基质金属蛋白酶抑制物－１（ＴＩＭＰ－１）ｍＲＮＡ的表达。结果模型组及依那普利组梗阻肾间质Ⅰ、Ⅲ、Ⅳ型胶原均明显增加，依那普利组比模型组的Ⅰ、Ⅲ、Ⅳ型胶原沉积减少（Ｐ＜０．００１），依那普利能明显减少肾间质中浸润的ＣＤ＋Ｔ淋巴细胞数（Ｐ＜０．０１），显著降低因输尿管结扎导致过度表达的α－ＳＭＡ、ＴＧＦ－β１ｍＲＮＡ、ＴＩＭＰ－１ｍＲＮＡ（Ｐ＜０．０１）。结论输尿管梗阻后ＣＤ８＋Ｔ淋巴细胞浸润肾间质，α－ＳＭＡ；ＴＧＦ－β１ｍＲＮＡ、ＴＩＭＰ－１ｍＲＮＡ表达增加，导致梗阻肾间质Ⅰ、Ⅲ、Ⅳ型胶原均明显增加，依那普利对其有一定的抑制作用。
Objective To study the mechanism of renal interstitial fibrosis after unilateral ureteral obstruction and the regulatory effect of enalapril, an angiotensin converting enzyme inhibitor. Methods Unilateral ureteral obstruction model was used to observe the expression of type Ⅰ, Ⅲ and type Ⅳ collagen, α-smooth muscle actin (α-SMA) and the number of T lymphocyte infiltration in obstructive renal interstitium 5 days after modeling by immunohistochemistry. The expression of transforming growth factor-β1 (TGF-β1) mRNA and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA in obstructive kidney tissue was detected by reverse transcription-polymerase chain reaction (RT- Results The collagen type Ⅰ, Ⅲ and Ⅳ in obstructive renal interstitium were significantly increased in the model group and the enalapril group. The deposition of type Ⅰ, Ⅲ and Ⅳ collagen in the enalapril group was less than that in the enalapril group (P <0.001) Enalapril significantly reduced the number of infiltrating CD + T lymphocytes in the renal interstitium (P <0.01), and significantly decreased the overexpression of α-SMA, TGF-β1mRNA and TIMP-1 mRNA (P <0. 01). Conclusions CD8 + T lymphocyte infiltration of renal interstitium, α-SMA, increased expression of TGF-β1mRNA and TIMP-1 mRNA after ureteral obstruction resulted in a significant increase of type Ⅰ, Ⅲ and Ⅳ collagen in obstructive renal interstitium, Inhibition.