重组人松弛素体外调节血管紧张素Ⅱ诱导的大鼠心肌纤维化

Recombinant human relaxin modulates angiotensin II-induced cardiac fibrosis

摘要: 目的: 观察在重组人松弛素（rhRLX）及血管紧张素Ⅱ（AngⅡ）作用下对心脏成纤维细胞功能（CFs）的影响。方法:原代培养Sprague-Dawley大鼠心脏成纤维细胞，经AngⅡ（10-6mmol/L）单独作用及AngⅡ加rhRLX(100μg/L)共同作用后，用MTT比色法测定CFs的增殖；用ELISA法检测Ⅰ型前胶原羧基末端肽（PⅠCP）和Ⅲ型前胶原氨基末端肽（PⅢNP）的水平。结果: rhRLX可显著抑制AngⅡ促进CFs增殖，并拮抗AngⅡ促进CFs分泌PⅠCP的作用。结论: rhRLX能够改善AngⅡ诱导的心肌纤维化。

Abstract: AIM: To observe the influence of recombinant human relaxin (rhRLX) on cardiac fibroblast (CF) functions under angiotensin II (AngII). METHODS: We cultured neonatal rat CFs in AngII (10-6 mmol/L) conditions in the absence or presence of rhRLX (100 μg/L). The cell growth of CF rate was determined by MTT colorimetry. Levels of procollagen type I C-terminal peptide (PICP) and procollagen type III amino terminal peptide (PIIINP) were detected by ELISA. RESULTS: rhRLX significantly inhibited the proliferation of cultured CF induced by AngII (P<0.01). AngII accelerated the production of PICP in CFs. rhRLX blocked collagen synthesis induced by AngII. CONCLUSION: rhRLX ameliorates cardiac fibrosis induced by AngII.