Feng Hong, Cao Jianlei, Zhang Guangyu, Wang Yanggan
Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei Province, China.
Planta Med. 2017 Jul;83(10):837-845. doi: 10.1055/s-0043-103415. Epub 2017 Feb 20.
Kaempferol has been demonstrated to provide benefits for the treatment of atherosclerosis, coronary heart disease, hyperlipidemia, and diabetes through its antioxidant and anti-inflammatory properties. However, its role in cardiac hypertrophy remains to be elucidated. The aim of our study was to investigate the effects of kaempferol on cardiac hypertrophy and the underlying mechanism. Mice subjected to aorta banding were treated with or without kaempferol (100 mg/kg/d, p. o.) for 6 weeks. Echocardiography was performed to evaluate cardiac function. Mice hearts were collected for pathological observation and molecular mechanism investigation. H9c2 cardiomyocytes were stimulated with or without phenylephrine for study. Kaempferol significantly attenuated cardiac hypertrophy induced by aorta banding as evidenced by decreased cardiomyocyte areas and interstitial fibrosis, accompanied with improved cardiac functions and decreased apoptosis. The ASK1/MAPK signaling pathways (JNK1/2 and p38) were markedly activated in the aorta banding mouse heart but inhibited by kaempferol treatment. In experiments, kaempferol also inhibited the activity of ASK1/JNK1/2/p38 signaling pathway and the enlargement of H9c2 cardiomyocytes. Furthermore, our study revealed that kaempferol could protect the mouse heart and H9c2 cells from pathological oxidative stress. Our investigation indicated that treatment with kaempferol protects against cardiac hypertrophy, and its cardioprotection may be partially explained by the inhibition of the ASK1/MAPK signaling pathway and the regulation of oxidative stress.
山奈酚已被证明通过其抗氧化和抗炎特性，对动脉粥样硬化、冠心病、高脂血症和糖尿病的治疗有益。然而，其在心肌肥大中的作用仍有待阐明。我们研究的目的是探讨山奈酚对心肌肥大的影响及其潜在机制。对接受主动脉缩窄的小鼠给予或不给予山奈酚（100mg/kg/d，口服）治疗6周。进行超声心动图检查以评估心脏功能。收集小鼠心脏进行病理观察和分子机制研究。用或不用去甲肾上腺素刺激H9c2心肌细胞进行研究。山奈酚显著减轻了主动脉缩窄诱导的心肌肥大，表现为心肌细胞面积减小和间质纤维化减轻，同时心脏功能改善，细胞凋亡减少。主动脉缩窄小鼠心脏中ASK1/MAPK信号通路（JNK1/2和p38）明显激活，但山奈酚治疗可抑制该通路。在实验中，山奈酚还抑制了ASK1/JNK1/2/p38信号通路的活性以及H9c2心肌细胞的增大。此外，我们的研究表明山奈酚可以保护小鼠心脏和H9c2细胞免受病理性氧化应激。我们的研究表明，山奈酚治疗可预防心肌肥大，其心脏保护作用可能部分归因于对ASK1/MAPK信号通路的抑制和对氧化应激的调节。
