Corilagin inhibits angiotensin II-induced atrial fibrosis and fibrillation in mice through the PI۳K-Akt pathway
Publish place: Iranian Journal of Basic Medical Sciences، Vol: 27، Issue: 6
Publish Year: 1403
نوع سند: مقاله ژورنالی
زبان: English
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شناسه ملی سند علمی:
JR_IJBMS-27-6_007
تاریخ نمایه سازی: 28 اسفند 1402
Abstract:
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.
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Authors
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
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