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Iranian Journal of Basic Medical Sciences، جلد ۲۷، شماره ۶، صفحات ۷۱۷-۷۲۴
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عنوان انگلیسی Corilagin inhibits angiotensin II-induced atrial fibrosis and fibrillation in mice through the PI3K-Akt pathway
چکیده انگلیسی مقاله 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: C57BL/6 mice (male, 8–10 weeks, n = 40) were subcutaneously infused either with saline or Ang II (2.0 mg/kg/day) and Cor (30 mg/kg) intraperitoneally injected 2 hr before Ang II infusion for 4 weeks. Mice were grouped into the control group (n=8), Cor group (n=8), Ang II group (n=8), and Ang II + Cor group (n=8). 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<0.001). In addition, Ang II + Cor significantly reduced Ang II-induced interleukin 1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-α) concentrations in atrial tissues. Furthermore, Cor significantly inhibited Ang II-induced p-PI3K, p-Akt, and NF-κB p-p65 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 PI3K-Akt pathway.
کلیدواژه‌های انگلیسی مقاله Akt, Angiotensin II, Atrial fibrillation, Atrial fibrosis, Corilagin, PI3K
نویسندگان مقاله | 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
نشانی اینترنتی https://ijbms.mums.ac.ir/article_23893.html
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