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目的:观察血管紧张素转换酶抑制剂(ACEI)对自发性高血压大鼠(spontaneously hypertensive rats,SHR)肾内肾素—血管紧张素系统(RAS)的影响,探讨盐酸贝那普利抗肾脏纤维化的机制.方法:应用病理检查、计算机分析、放射免疫、分光光度法和逆转录—聚合酶链式反应等方法,检测贝那普利组(SHR-B)、SHR组(SHR)及对照Wistar-Kyoto组(WKY)大鼠肾脏间质胶原面积、肾脏血管紧张素转换酶(ACE)活性、肾脏局部血管紧张素II(Ang II)水平及肾脏组织I,III型胶原mRNA表达.结果:SHR-B组肾脏胶原面积比SHR组明显减少(P<0.01).SHR-B组肾皮质提取液ACE活性为(28±6)nmol/(min·g),SHR组为(53±8)nmol/(min·g),WKY组为(25±7)nmol/(min·g).SHR-B组肾皮质提取液ACE活性比SHR组明显降低(P<0.01),但与WKY组相比,无显著差异.SHR-B组肾皮质组织匀浆液Ang II水平为(49±16)ng/g,SHR组为(83±8)ng/g,WKY组为(43±14)ng/g.SHR-B组肾皮质组织匀浆液Ang II水平比SHR组明显降低(P<0.01),但与WKY相比无显著差异(P>0.05).SHR-B组肾脏组织I型胶原及III型胶原mRNA表达相对含量也均明显低于SHR组(P均<0.01).结论:贝那普利可通过减少肾脏胶原的合成和抑制肾内的RAS而减轻肾脏的纤维化.
Objective: To observe the effect of angiotensin converting enzyme inhibitor (ACEI) on renal renin-angiotensin system (RAS) in spontaneously hypertensive rats (SHR) (SHR-B), SHR group (SHR) and control group (SHR group) .Methods: Pathological examination, computer analysis, radioimmunoassay, spectrophotometry and reverse transcription-polymerase chain reaction were used to detect the expression of SHR- Control Wistar-Kyoto group (WKY) rat kidney interstitial collagen area, renal angiotensin-converting enzyme (ACE) activity, renal local angiotensin II (Ang II) levels and kidney tissue type I and type III collagen mRNA expression.Results : Compared with SHR group, the area of renal collagen in SHR-B group was significantly decreased (P <0.01) .The ACE activity in SHR-B group was (28 ± 6) nmol / (min · g) (25 ± 7) nmol / (min · g) in WKY group.The ACE activity of renal cortex extract in SHR-B group was significantly lower than that in SHR group (P <0.01) (49 ± 16) ng / g in SHR-B group compared with (83 ± 8) ng / g in SHR group and (43 ± 14) ng / g in WKY group / g.SHR- B group renal cortical tissue homogenate Ang II water (P <0.01), but no significant difference compared with WKY (P> 0.05) .The relative content of type I collagen and type III collagen mRNA in SHR-B group was also significantly lower than that in SHR group P <0.01) .Conclusion: Benazepril can reduce renal fibrosis by reducing renal collagen synthesis and inhibiting intrarenal RAS.