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Kaempferol Inhibits Myocardial Fibrosis by Downregulating FVII
Ming Zhang1, Zhengbo Zhu2, Qian Zhou3
1Anhui Medical College.
Abstract:
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.
Insights
Kaempferol (KMP) effectively treats myocardial fibrosis by improving heart function and reducing inflammation. KMP downregulates coagulation factor VII (FVII), offering a potential therapy for heart conditions.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Biochemistry
Background:
- Myocardial fibrosis is a key factor in heart failure progression.
- Kaempferol (KMP), a natural flavonoid, possesses antioxidant and anti-inflammatory properties.
- Understanding KMP's role in mitigating myocardial fibrosis is crucial.
Purpose of the Study:
- To investigate the therapeutic effects of Kaempferol (KMP) on isoproterenol-induced myocardial fibrosis.
- To elucidate the molecular mechanisms underlying KMP's cardioprotective actions.
Main Methods:
- Myocardial fibrosis model induced by isoproterenol injection in mice.
- Cardiac function assessed via echocardiography.
- Histological analysis (Masson, Sirius red), immunohistochemistry (α-SMA, Collagen III), RT-qPCR, ELISA, and Western blot were employed.
Main Results:
- KMP treatment significantly improved cardiac function and suppressed myocardial fibrosis.
- KMP decreased fibrosis-related gene expression and attenuated inflammation.
- KMP inhibited the overexpression of coagulation factor VII (FVII), which is linked to fibrosis and inflammation.
Conclusions:
- Kaempferol (KMP) demonstrates protective effects against myocardial fibrosis.
- KMP exerts its benefits by downregulating coagulation factor VII (FVII).
- KMP presents a promising therapeutic candidate for treating myocardial fibrosis and related cardiovascular diseases.
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