Zhou C, Li J, Wang H
Department of Nephrology, First Hospital, Beijing Medical University, Beijing 100034.
Zhonghua Nei Ke Za Zhi. 1999 Jan;38(1):44-6.
To explore the possible mechanism of benazepril in diminishing the progression of the renal diseases.
Experimental glomerulosclerosis in rats was induced by adriamycin. The treated group was given benazepril (4 mg x kg(-1) x 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 beta1 (TGF beta1) and extracellular matrix (ECM) examination. To observe the expression of TGFbeta1 mRNA in the kidney, in situ hybridization was performed.
In the rats treated with benazeapril, ACE activity and Ang II concentration in renal tissue were significantly inhibited. In the meantime, expression of TGFbeta1 mRNA and TGFbeta1 protein were down-regulated, accompanied by decreasing accumulation of ECM (compared with the untreated rats, P < 0.01).
Benazepril plays an important role in down-regulating the expression of TGFbeta1 and decreasing the accumulation of ECM by blocking intrarenal renin-angiotensin system.
探讨贝那普利延缓肾脏疾病进展的可能机制。
采用阿霉素诱导大鼠实验性肾小球硬化。治疗组给予贝那普利（4mg·kg⁻¹·d⁻¹）。分别用比色法和放射免疫法测定肾内血管紧张素转换酶（ACE）活性和血管紧张素II（AngII）浓度。采用免疫组织化学染色检测转化生长因子β1（TGFβ1）和细胞外基质（ECM）。用原位杂交法观察肾脏中TGFβ1 mRNA的表达。
贝那普利治疗的大鼠肾组织中ACE活性和Ang II浓度明显受到抑制。同时，TGFβ1 mRNA和TGFβ1蛋白的表达下调，伴有ECM积聚减少（与未治疗大鼠相比，P<0.01）。
贝那普利通过阻断肾内肾素-血管紧张素系统，在下调TGFβ1表达和减少ECM积聚方面发挥重要作用。
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