Yang Xiaofang, Zheng Xuebin, Xiao Xiangqian, Li Li
Changsha Fourth Hospital - Department of Cardiology - Changsha - Hunan - China.
Acta Cir Bras. 2024 Sep 30;39:e396524. doi: 10.1590/acb396524. eCollection 2024.
This work aimed to investigate the effects of Tanshinone IIA (Tan IIA) on myocardial cell (MC) apoptosis in a rat model of heart failure (HF).
Tan IIA was extracted from Salvia miltiorrhiza Bunge (SMB) using an ethanol reflux method. Fifty rats were randomly divided into five groups: sham (no treatment), mod (HF model establishment), low dose (LD: 0.1 mL/kg Tan IIA), medium dose (MD: 0.3 mL/kg Tan IIA), and high dose (HD: 0.5 mL/kg Tan IIA), with 10 rats in each group. The effects of different doses of Tan IIA on cardiac function, MC apoptosis, and the levels of proteins associated with the PI3K/Akt/mTOR signaling pathway were compared.
Mod group showed a significant decrease in systolic arterial pressure, mean arterial pressure, heart rate, left ventricular systolic pressure, left ventricular ejection fraction, left ventricular fractional shortening, and the levels of p-PI3K, p-Akt, and p-mTOR proteins versus sham group (p < 0.05). Additionally, the left ventricular end-diastolic diameter (LVIDd), end-systolic diameter, diastolic pressure, and MC apoptosis were significantly increased (p < 0.05). LD, MD, and HD groups exhibited significant improvements across various indicators of cardiac function and MC apoptosis versus mod group (p < 0.05).
Tan IIA may improve cardiac function and inhibit MC apoptosis in rats with HF by modulating the PI3K/Akt/mTOR signaling pathway.
本研究旨在探讨丹参酮IIA(Tan IIA)对心力衰竭(HF)大鼠模型心肌细胞(MC)凋亡的影响。
采用乙醇回流法从丹参中提取Tan IIA。50只大鼠随机分为五组:假手术组(未处理)、模型组(建立HF模型)、低剂量组(LD:0.1 mL/kg Tan IIA)、中剂量组(MD:0.3 mL/kg Tan IIA)和高剂量组(HD:0.5 mL/kg Tan IIA),每组10只大鼠。比较不同剂量Tan IIA对心脏功能、MC凋亡以及与PI3K/Akt/mTOR信号通路相关蛋白水平的影响。
与假手术组相比,模型组的收缩压、平均动脉压、心率、左心室收缩压、左心室射血分数、左心室短轴缩短率以及p-PI3K、p-Akt和p-mTOR蛋白水平显著降低(p < 0.05)。此外,左心室舒张末期内径(LVIDd)、收缩末期内径、舒张压和MC凋亡显著增加(p < 0.05)。与模型组相比,LD、MD和HD组在心脏功能和MC凋亡的各项指标上均有显著改善(p < 0.05)。
Tan IIA可能通过调节PI3K/Akt/mTOR信号通路改善HF大鼠的心脏功能并抑制MC凋亡。