Objective: To explore the effect of hesperetin (HES) on collagen expression in cardiac fibroblasts in vitro induced by angiotensin II (AngII).
Methods: Cell growth was determined by trypan blue staining, reactive oxygen species (ROS) generation by microplate reader, the expressions of collagen I,III and matrix metalloproteinase 1 (MMP-1) by real-time polymerase chain reaction (PCR) and cell proliferation by cell counting kit-8.
Results: HES and AngII+HES had no effect on cellular activity. AngII significantly increased ROS generation (1.70 ± 0.12 vs 1, P < 0.01), gene expression of collagen I,III both increased (1.31 ± 0.08 vs 1, 1.40 ± 0.09 vs 1, both P < 0.01) while MMP-1 decreased (0.68 ± 0.03 vs 1, P < 0.01). Ang II also induced the proliferation of fibroblasts (1.91 ± 0.18 vs 1, P < 0.01). While HES (25, 50, 100 µmol/L) or NAC (1 mmol/L) reversed these effects during co-treating with AngII, ROS decreased versus the Ang II group(1.37 ± 0.05, 1.16 ± 0.08, 1.07 ± 0.07, 1.12 ± 0.07 vs 1.70 ± 0.12, all P < 0.01) , gene expression of collagenI,III also decreased (1.22 ± 0.08 and 1.27 ± 0.07, 1.14 ± 0.07 and 1.00 ± 0.06, 1.02 ± 0.06 and 0.99 ± 0.05, 1.08 ± 0.07 and 1.09 ± 0.06 vs 1.31 ± 0.08 and 1.40 ± 0.09, all P < 0.01), MMP-1 increased (0.76 ± 0.05, 0.88 ± 0.07, 1.01 ± 0.08, 0.96 ± 0.07 vs 0.68 ± 0.03, P < 0.01) versus the Ang II group. Cell proliferation was also inhibited (1.42 ± 0.07, 1.38 ± 0.03, 1.07 ± 0.15, 1.16 ± 0.11 vs 1.91 ± 0.18, all P < 0.01). NAC had the same effect with HES.
Conclusion: HES inhibits the synthesis of collagen and the Ang II-induced proliferation of fibroblast through suppressing the ROS generation.