研究动态
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Salidroside 通过抑制 LOXL2-TGF-β1-Smad2/3 通路来减轻血管紧张素-II 引起的心房纤维化和心房颤动脆弱性。

Salidroside attenuates atrial fibrosis and atrial fibrillation vulnerability induced by angiotensin-II through inhibition of LOXL2-TGF-β1-Smad2/3 pathway.

发表日期:2023 Nov
作者: Zhen Hai, Yingbiao Wu, Zhongping Ning
来源: ANTIOXIDANTS & REDOX SIGNALING

摘要:

红景天苷 (SAL) 是从中国植物玫瑰红景天中分离出来的活性成分,具有抗炎、抗氧化、抗癌、神经保护和肾脏保护特性。血管紧张素 II (Ang II) 引起的心房纤维化在心房颤动 (AF) 的发生过程中发挥着至关重要的作用。本研究调查了 SAL 在 AF 中的参与、其对 AF 的脆弱性以及 Ang II 诱导的炎症性心房纤维化。将 Ang II(2 毫克/公斤/天)注入雄性 C57BL/6 小鼠(8-10 周)皮下老,n = 40)花了四个星期来创建 AF 模型。 SAL(50 mg/kg/天)每天腹腔注射一次,持续 28 天。进行形态学、组织学和生化分析。在体内使用经食管突发起搏来诱导 AF。Ang II 注射增加了小鼠的心率和收缩压 (SBP),而 SAL 治疗则显着降低。 Ang II 输注增加了小鼠的左心房直径 (LAD),而 SAL 治疗后左心房直径 (LAD) 减弱。单独使用 SAL 并不影响 AF 诱导性,但 SAL 治疗显着降低 Ang II 诱导的 AF 诱导性。此外,SAL 治疗小鼠体内白细胞介素 1 β (IL-1β)、白细胞介素 6 (IL-6) 和肿瘤坏死因子 α (TNF-α) 的表达水平受到抑制。与 Ang II 组相比,Ang II 输注提高了丙二醛 (MDA) 水平并降低了超氧化物歧化酶 (SOD) 和过氧化氢酶 (CAT) 活性,但 SAL 治疗改变了所有这些效应。与 Ang II 组小鼠相比,SAL 治疗显着降低了 LOXL2、TGF-β1、p-Smad2 和 p-Smad3 蛋白表达。SAL 抑制心房纤维化,并通过抑制 LOXL2-TGF-β1-Smad2/3 通路潜在减弱房颤易感性增加.© 2023 作者。
Salidroside (SAL), an active component isolated from the Chinese plant Rose Rhodiola, has anti-inflammatory, antioxidant, anti-cancer, neuroprotective, and renal protective properties. Atrial fibrosis developed due to angiotensin II (Ang II) plays a crucial function in developing atrial fibrillation (AF). This research investigates the involvement of SAL in AF, its vulnerability to AF, and Ang II-induced inflammatory atrial fibrosis.Ang II (2 mg/kg/day) was infused underneath the skin into male C57BL/6 mice (8-10 weeks old, n = 40) for four weeks to create the AF model. SAL (50 mg/kg/day) was given intraperitoneally once per day for 28 days. Analyses of morphology, histology, and biochemical were carried out. Transesophageal burst pacing was used in vivo to induce AF.Ang II injection increased mice's heart rate and systolic blood pressure (SBP), whereas SAL treatment was significantly reduced. Ang II infusion increased left atrial diameter (LAD) in mice, which was attenuated after SAL treatment. SAL alone did not affect AF inducibility, but SAL therapy markedly decreased Ang II-induced AF inducibility. Additionally, the expression levels of interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were inhibited with SAL therapy in mice. Compared to the Ang II group, Ang II infusion raised malondialdehyde (MDA) levels and reduced superoxide dismutase (SOD) and catalase (CAT) activity, but SAL therapy altered all of these effects. SAL treatment significantly reduced LOXL2, TGF-β1, p-Smad2 and p-Smad3 protein expression than the Ang II group mice.SAL inhibits atrial fibrosis and potentially attenuates increased susceptibility to AF by suppressing the LOXL2-TGF-β1-Smad2/3 pathway.© 2023 The Authors.