论文部分内容阅读
目的：探讨血管紧张素Ⅱ受体在系统性红斑狼疮发病中的作用。方法：利用逆转录聚合酶链反应（ＲＴＰＣＲ）的方法检测ＭＲＬｌｐｒ／ｌｐｒ自发狼疮鼠和ＭＲＬ系小鼠８和１８周时肾、心、肺、肝、脑、垂体、肾上腺、睾丸、卵巢和子宫组织中血管紧张素ⅡＡＴ１Ａ、ＡＴ１Ｂ和ＡＴ２受体的基因表达。结果：在１８周龄ＭＲＬｌｐｒ／ｌｐｒ小鼠肾、心、肺、肝、脑和睾丸等明显受损伤的组织中，ＡＴ１Ａ受体的ｍＲＮＡ表达有显著升高，而ＡＴ１Ｂ和ＡＴ２受体的基因表达与ＭＲＬ小鼠８和１８周时及ＭＲＬｌｐｒｌ／ｌｐｒ小鼠末发病（８周龄）时比较则无明显改变。应用血管紧张素转化酶抑制剂盐酸苯那普利治疗后，１８周龄ＭＲＬｌｐｒ／ｌｐｒ小鼠的尿蛋白和肾、心、肺、肝、脑和睾丸组织中ＡＴ１Ａ受体的ｍＲＮＡ水平显著降低，但上述脏器的病理损伤无明显减轻。结论：ＡＴ１Ａ受体参与了狼疮导致的多脏器损伤过程并起到一定作用。
Objective: To investigate the role of angiotensin Ⅱ receptor in the pathogenesis of systemic lupus erythematosus. Methods: Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression levels of kidney, heart, lung, liver, brain, pituitary, adrenal, testis, Gene expression of angiotensin II AT1A, AT1B and AT2 receptors in ovarian and uterine tissues. RESULTS: The mRNA expression of AT1A receptor was significantly increased in the tissues of obviously injured kidney, heart, lung, liver, brain and testis of MRLlpr / lpr mice of 18 weeks old, but the gene expressions of AT1B and AT2 receptors There were no significant changes compared to the MRL mice at the 8th and 18th weeks and at the end of the MRLlprl / lpr mice (8 weeks old). After treatment with benazepril hydrochloride, an angiotensin converting enzyme inhibitor, urinary protein and mRNA levels of AT1A receptors in kidney, heart, lung, liver, brain and testis tissue of 18 week old MRLlpr / lpr mice were significantly reduced, However, the pathological organ damage was not significantly reduced. Conclusion: AT1A receptor participates in the process of multiple organ injury caused by lupus and plays a role.