Xiaogang Zhang - Cardiovascular Department, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, China
Bei Tian - Cardiovascular Department, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, China
Xinpeng Cong - Cardiovascular Department, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, China
Zhongping Ning - Cardiovascular Department, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, China

Objective(s): Corilagin (Cor) is reported as beiing hepatoprotective, anti-inflammatory, antibacterial, and anti-oxidant, while the effect on atrial fibrosis remains unknown. Therefore, we investigated the protective effect of Cor in angiotensin II (Ang II)-induced atrial fibrosis and atrial fibrillation (AF).Materials and Methods: C۵۷BL/۶ mice (male, ۸–۱۰ weeks, n = ۴۰) were subcutaneously infused either with saline or Ang II (۲.۰ mg/kg/day) and Cor (۳۰ mg/kg) intraperitoneally injected ۲ hr before Ang II infusion for ۴ weeks. Mice were grouped into the control group (n=۸), Cor group (n=۸), Ang II group (n=۸), and Ang II + Cor group (n=۸). Morphological, histological, and biochemical examinations were performed. In vivo, transesophageal burst pacing was used to generate AF.Results: Cor treatment markedly reduced Ang II-induced AF development in mice. Ang II + Cor therapy potentially decreased the atrial fibrotic area. It significantly decreased the increase in smooth muscle alpha-actin (α-SMA), CTGF, Collagen I, and Collagen III expressions brought on by Ang II treatment. Moreover, Ang II + Cor treatment remarkably decreased the malondialdehyde (MDA) content, whereas superoxide dismutase (SOD) and catalase (CAT) activities were potentially increased (all, P<۰.۰۰۱). In addition, Ang II + Cor significantly reduced Ang II-induced interleukin ۱ beta (IL-۱β), interleukin ۶ (IL-۶), and tumor necrosis factor-alpha (TNF-α) concentrations in atrial tissues. Furthermore, Cor significantly inhibited Ang II-induced p-PI۳K, p-Akt, and NF-κB p-p۶۵ protein expression in atrial tissues. Conclusion: Our data speculated that Cor could have a protective effect against Ang II-induced atrial fibrosis and AF via down-regulation of the PI۳K-Akt pathway.

Akt, Angiotensin II, Atrial fibrillation, Atrial fibrosis, Corilagin, PI۳K