Department of Cardiovascular Medicine, Chengde Medical University Affiliated Hospital, Chengde, China.
Cell Mol Biol (Noisy-le-grand). 2023 Sep 30;69(9):234-238. doi: 10.14715/cmb/2023.69.9.36.
To uncover the potential effect of Perindopril on cardiac fibrosis caused by pressure overload and the underlying mechanism. Cardiac fibrosis model in mice was established by TAC method. Mice were assigned into sham group, TAC group, 2 mg/kg Perindopril group (Per (2 mg/kg)) and 8 mg/kg Perindopril group (Per (8 mg/kg)). Cardiac structure changes were assessed by measuring HW/BW, HW/TBL, LW/BW and LW/TBL in each group. Echocardiography was performed to assess mouse cardiac function by recording EF, LVIDd, IVSd and LVPWd. Relative levels of fibrosis markers were determined. AngII content was examined by ELISA. Besides, mRNA levels of key genes in the AngII/AT1R pathway were finally detected. TAC induced cardiac insufficiency, left ventricular dilatation, cardiac hypertrophy and myocardial collagen deposition in mice. In addition, fibrosis markers were upregulated in mice of TAC group. Perindopril markedly reversed TAC-induced pathological changes in cardiac structure and function of mice. Meanwhile, Perindopril dose-dependently reversed the upregulated genes in the AngII/AT1R pathway. Perindopril improves cardiac fibrosis induced by pressure overload through activating the AngII/AT1R pathway.
为了揭示培哚普利对压力超负荷引起的心脏纤维化的潜在作用及其潜在机制。通过 TAC 方法建立了小鼠心脏纤维化模型。将小鼠分为假手术组、TAC 组、2mg/kg 培哚普利组（Per（2mg/kg））和 8mg/kg 培哚普利组（Per（8mg/kg））。通过测量每组的 HW/BW、HW/TBL、LW/BW 和 LW/TBL 来评估心脏结构变化。通过记录 EF、LVIDd、IVSd 和 LVPWd 来进行超声心动图检查，以评估小鼠的心脏功能。测定纤维化标志物的相对水平。通过 ELISA 检测 AngII 含量。最后，检测 AngII/AT1R 通路中关键基因的 mRNA 水平。TAC 诱导小鼠心功能不全、左心室扩张、心肌肥厚和心肌胶原沉积。此外，TAC 组的纤维化标志物表达上调。培哚普利明显逆转了 TAC 诱导的小鼠心脏结构和功能的病理性变化。同时，培哚普利呈剂量依赖性逆转 AngII/AT1R 通路中上调的基因。培哚普利通过激活 AngII/AT1R 通路改善压力超负荷引起的心脏纤维化。
