Substance Abuse Pharmacology Group, Korea Institute of Toxicology, KRICT, Daejeon 34114, Korea.
Division of Cardiovascular Surgery, Department of Thoracic and Cardiovascular Surgery, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul 03722, Korea.
Molecules. 2020 Nov 12;25(22):5279. doi: 10.3390/molecules25225279.
Pathological cardiac hypertrophy is characterized by an abnormal increase in cardiac muscle mass in the left ventricle, resulting in cardiac dysfunction. Although various therapeutic approaches are being continuously developed for heart failure, several studies have suggested natural compounds as novel potential strategies. Considering relevant compounds, we investigated a new role for Pterosin B for which the potential life-affecting biological and therapeutic effects on cardiomyocyte hypertrophy are not fully known. Thus, we investigated whether Pterosin B can regulate cardiomyocyte hypertrophy induced by angiotensin II (Ang II) using H9c2 cells. The antihypertrophic effect of Pterosin B was evaluated, and the results showed that it reduced hypertrophy-related gene expression, cell size, and protein synthesis. In addition, upon Ang II stimulation, Pterosin B attenuated the activation and expression of major receptors, Ang II type 1 receptor and a receptor for advanced glycation end products, by inhibiting the phosphorylation of PKC-ERK-NF-κB pathway signaling molecules. In addition, Pterosin B showed the ability to reduce excessive intracellular reactive oxygen species, critical mediators for cardiac hypertrophy upon Ang II exposure, by regulating the expression levels of NAD(P)H oxidase 2/4. Our results demonstrate the protective role of Pterosin B in cardiomyocyte hypertrophy, suggesting it is a potential therapeutic candidate.
病理性心肌肥厚的特征是左心室心肌质量异常增加，导致心脏功能障碍。尽管正在不断开发各种心力衰竭的治疗方法，但有几项研究表明，天然化合物是一种新的潜在策略。考虑到相关化合物，我们研究了 Pterosin B 的新作用，而其对心肌肥厚的潜在影响生命的生物学和治疗作用尚不完全清楚。因此，我们研究了 Pterosin B 是否可以调节血管紧张素 II（Ang II）诱导的心肌细胞肥大，用 H9c2 细胞进行了研究。评估了 Pterosin B 的抗肥大作用，结果表明它降低了与肥大相关的基因表达、细胞大小和蛋白质合成。此外，在 Ang II 刺激下，Pterosin B 通过抑制蛋白激酶 C-细胞外信号调节激酶-核因子 κB 通路信号分子的磷酸化，减弱了主要受体，即血管紧张素 II 型 1 受体和晚期糖基化终产物受体的激活和表达。此外，Pterosin B 还显示出通过调节 NAD（P）H 氧化酶 2/4 的表达水平，减少在 Ang II 暴露时对心脏肥厚至关重要的细胞内活性氧物质的能力。我们的研究结果表明 Pterosin B 在心肌肥厚中的保护作用，提示其可能是一种潜在的治疗候选药物。
