Recombinant human relaxin modulates angiotensin II-induced cardiac fibrosis

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.