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Capillarisin Pretreatment Inhibits Oxidative Stress and Inflammation in Rats After Myocardial Infarction Induction

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Abstract

Myocardial infarction is a type of cardiovascular disease that leads to the loss of cardiomyocyte and cardiac dysfunction and is classified as the leading cause of death. This study investigated the effect of capillarisin, a bioactive ingredient of Artemisia capillaris Thunb., Asteraceae, root extracts, on myocardial infarction development in a rat model. Capillarisin treatment lessened the myocardial infarct size and improved cardiac function in myocardial infarction rats by lowering creatine kinase-MB, lactate dehydrogenase, and malondialdehyde levels, and elevating the level of superoxide dismutase in serum, suggesting its inhibitory effect on oxidative stress. Capillarisin also inhibited inflammation and cardiomyocyte apoptosis in myocardial tissues. The decreased protein levels of phosphatidylinositol 3-kinase and phosphorylation of protein kinase B in myocardial infarction rats were upregulated by capillarisin treatment. Capillarisin reduced the cardiomyocyte apoptosis and mitigated oxidative stress and inflammation in myocardial infarction rats by activating phosphatidylinositol 3-kinase and phosphorylation of protein kinase B signaling pathway.

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Authors

Contributions

BR, SQ, and YW designed the study. BR and SQ performed the research method and analyzed the data. YW wrote the paper. BR and SQ were responsible for polishing the manuscript. All the authors have discussed the results and approved the final manuscript.

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Correspondence to Yayun Wang.

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This experiment was reviewed by the Animal Ethics Committee of Hubei Provincial Center for Disease Control and Prevention (approval number: 202220012). All experimental were conducted in accordance with the National Institutes of Health (NIH) Guide for the Care and Use of Laboratory Animals.

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Ruan, B., Qiu, S. & Wang, Y. Capillarisin Pretreatment Inhibits Oxidative Stress and Inflammation in Rats After Myocardial Infarction Induction. Rev. Bras. Farmacogn. 32, 984–992 (2022). https://doi.org/10.1007/s43450-022-00306-1

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  • DOI: https://doi.org/10.1007/s43450-022-00306-1

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