摘要
目的探讨苯那普利延缓肾脏疾病进展的可能作用机制。方法采用实验性肾小球硬化模型，治疗组给苯那普利（４ｍｇ·ｋｇ－１·ｄ－１）。用比色法和放免法分别测定肾内血管紧张素转换酶（ＡＣＥ）活性和血管紧张素Ⅱ（ＡｎｇⅡ）含量，免疫组化检测肾组织转化生长因子β１（ＴＧＦβ１）和细胞外基质（ＥＣＭ），原位杂交观察ＴＧＦβ１ｍＲＮＡ表达。结果治疗组肾内ＡＣＥ活性和ＡｎｇⅡ与非治疗组比较，受到明显抑制（Ｐ＜０．０１）。治疗组肾小球和肾小管区ＴＧＦβ１ｍＲＮＡ表达量显著低于非治疗组（Ｐ＜００１）。同时，ＥＣＭ在肾小球内沉积也较非治疗组显著减少（Ｐ＜０．０１）。结论苯那普利通过阻断肾内肾素血管紧张素系统，在下调ＴＧＦβ１表达和ＥＣＭ积聚中起重要作用。
Objective To explore the possible mechanism of benazepril in diminishing the progression of the renal diseases. Methods Experimental glomerulosclerosis in rats was induced by adriamycin. The treated group was given benazepril (4 mg·kg -1 ·d -1 ). Intrarenal angiotensin converting enzyme (ACE) activity and angiotensin Ⅱ (AngⅡ) concentration were measured with colorimetry and radioimmunoassay respectively. Immunohistochemistry staining was employed for transforming growth factor β1 (TGF β1) and extracellular matrix (ECM) examination. To observe the expression of TGFβ1 mRNA in the kidney, in situ hybridization was performed. Results In the rats treated with benazeapril, ACE activity and Ang Ⅱ concentration in renal tissue were significantly inhibited. In the meantime, expression of TGFβ1 mRNA and TGFβ1 protein were down regulated, accompanied by decreasing accumulation of ECM (compared with the untreated rats, P <0.01). Conclusion Benazepril plays an important role in down regulating the expression of TGFβ1 and decreasing the accumulation of ECM by blocking intrarenal reninangiotensin system.
出处
《中华内科杂志》
CAS
CSCD
北大核心
1999年第1期44-46,I002,共3页
Chinese Journal of Internal Medicine
关键词
苯那普利
肾疾病
RAS
ANGⅡ
ECM
Angiotensin converting enzyme inhibitors
Renin angiotensin system
Transforming growth factor beta
Glomerulosclerosis focal
