GUT:肾素-血管紧张素系统(RAS)与炎症性肠病

2019-08-21 MedSci MedSci原创

研究认为RAS介导人类细胞的纤维化并在肠道炎症中受到干扰,靶向该系统的药物与改善疾病结局有关

近日研究人员评价了肾素-血管紧张素系统(RAS)对肠道炎症和纤维化的影响。

高血压患者采用血管紧张素(Ang)II和Ang(1-7),其受体拮抗剂坎地沙坦、A779以及ACE抑制剂卡托普利治疗后,研究人员对培养的人结肠肌纤维细胞增殖和胶原分泌进行评估。对有和无IBD患者的循环和肠道RAS成分进行了评估。回顾性研究评估了应用ACE抑制剂和血管紧张素受体阻滞剂(ARBs)治疗的IBD患者的疾病结局。

Ang(1-7)以剂量依赖性方式减少人结肠肌纤维细胞增殖,Ang II轻微但不显著增加增殖,坎地沙坦逆转了这种作用。Ang(1-7)和卡托普利可降低结肠成纤维细胞胶原的分泌,而AngⅡ则显著增加。IBD患者的循环肾素(平均25.4 vs 18.6 mIU/L)和ACE2/ACE比值(平均0.92 vs 0.69)高于无IBD的对照组。在健康和患病的肠道中鉴定出RAS基因转录和肽。结肠粘膜Masson's三色染色与Ang II相关,与ACE2活性呈负相关。与不需要手术或住院的患者相比,需要手术治疗(1/37 vs 12/75,p=0.034)和住院治疗(0.034/34 vs 8/68,p=0.049)超过2年的IBD患者使用ACE抑制剂和ARBS治疗的频率较低。

研究认为RAS介导人类细胞的纤维化并在肠道炎症中受到干扰,靶向该系统的药物与改善疾病结局有关。

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