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多种慢性肾脏疾病的共同病理特征是肾小球及肾小管间质的纤维化 ,转化生长因子 β(TGF β)和血管紧张素Ⅱ (AngⅡ )都是这一过程中有重要意义的生物活性因子。近年发现 ,AngⅡ与TGF β之间有密切的相互作用关系。在体外 ,AngⅡ可诱导肾近曲小管上皮细胞及系膜细胞TGF β的表达 ;对多种慢性肾病动物模型的研究发现 ,这种作用在体内同样存在。用血管紧张素转换酶抑制药 (ACEI)或 (和 )血管紧张素Ⅱ 1型受体阻滞药(AT1RA)阻断AngⅡ的作用可使肾内TGF β表达下降 ,但不能使之完全恢复正常 ,因而只能延缓而不能阻止疾病的进展。而在传统治疗的基础上合用TGF β的特异性阻滞药 ,有可能真正阻断肾病的进展。
The common pathological features of a variety of chronic kidney diseases are glomerular and tubular interstitial fibrosis. Transforming growth factor beta (TGF beta) and angiotensin II (Ang II) are both important biological activities in this process factor. In recent years, it has been found that there is a close interaction between AngⅡ and TGFβ. In vitro, Ang II induced the expression of TGFβ in renal proximal tubule epithelial cells and mesangial cells. The study on various animal models of chronic kidney disease found that this effect exists in vivo. Angiotensin converting enzyme inhibitor (ACEI) or (and) angiotensin Ⅱ type 1 receptor blocker (AT1RA) blocking the role of Ang Ⅱ can reduce renal TGFβ expression, but can not make it fully restored to normal , It can only be delayed but can not stop the progress of the disease. In the traditional treatment based on the combination of specific TGF β blocking drugs, may truly block the progress of kidney disease.