心肌纤维化
纤维化
免疫印迹
炎症
心肌梗塞
天狼星红
免疫组织化学
心脏纤维化
心功能曲线
心力衰竭
细胞因子
药理学
医学
肿瘤坏死因子α
山奈酚
细胞凋亡
氧化应激
实时聚合酶链反应
病态的
基因表达
癌症研究
p38丝裂原活化蛋白激酶
促炎细胞因子
化学
逆转录聚合酶链式反应
组织学
抗氧化剂
内科学
血管生成
作者
Mingyu Zhang,Zunmin Zhu,Qian Zhou,Liyun Liu
标识
DOI:10.1615/critreveukaryotgeneexpr.v35.i6.10
摘要
Myocardial fibrosis is a critical pathological process in the progression of heart failure and other cardiovascular diseases. Kaempferol (KMP), a natural flavonoid, has antioxidant and anti-inflammatory properties. This study investigates the effects of KMP on myocardial fibrosis. Isoproterenol injection was used to establish myocardial fibrosis mouse model. Cardiac function was assessed by echocardiography. Histology analysis was conducted using Masson assay and Sirius red staining. The expression of survival of motor neuron 1 (α-SMA) and Collagen III was detected using immunohistochemistry. RNA expression was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cytokine release was detected using enzyme-linked immunosorbent assay. Protein expression was detected using Western blot. We found that KMP treatment improved cardiac function as well as suppressed myocardial fibrosis. Moreover, KMP treatment decreased expression of fibrosis-related genes and attenuated inflammation in fibrotic hearts. Furthermore, KMP treatment inhibited the expression of coagulation factor VII (FVII), the overexpression of which promoted inflammation response and myocardial fibrosis. In summary, KMP exerts protective effects against myocardial fibrosis via downregulating FVII. These findings suggest that KMP may be a promising therapeutic candidate for myocardial fibrosis.
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