■据报道,Corilagin(Cor)具有保肝作用,抗炎,抗菌,和抗氧化剂,而对心房纤维化的影响尚不清楚。因此,我们研究了Cor对血管紧张素II(AngII)诱导的心房纤维化和心房颤动(AF)的保护作用.
■C57BL/6小鼠(雄性,8-10周,n=40)皮下输注盐水或AngII(2.0mg/kg/天),并在AngII输注前2小时腹膜内注射Cor(30mg/kg),持续4周。小鼠分为对照组(n=8),Cor组(n=8),AngII组(n=8),AngⅡ+Cor组(n=8)。形态学,组织学,并进行生化检查。在体内,经食管猝发起搏用于产生AF。
■Cor治疗显著减少了AngII诱导的小鼠AF发展。AngII+Cor治疗可能减少心房纤维化面积。它显著降低了平滑肌α-肌动蛋白(α-SMA)的增加,CTGF,胶原蛋白I,和AngII治疗带来的胶原蛋白III表达。此外,AngII+Cor处理显著降低了丙二醛(MDA)含量,而超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性潜在地增加(所有,P<0.001)。此外,AngII+Cor显著降低AngII诱导的白细胞介素1β(IL-1β),白细胞介素6(IL-6),和心房组织中肿瘤坏死因子-α(TNF-α)的浓度。此外,Cor显著抑制AngII诱导的p-PI3K,p-Akt,和NF-κBp-p65蛋白在心房组织中的表达。
■我们的数据推测Cor可能通过下调PI3K-Akt通路对AngII诱导的心房纤维化和房颤具有保护作用。
UNASSIGNED: 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).
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.