4.7 Article

Immunomodulatory effects of icariin in a myocardial infarction mouse model

期刊

BIOENGINEERED
卷 13, 期 5, 页码 12504-12515

出版社

TAYLOR & FRANCIS INC
DOI: 10.1080/21655979.2022.2076453

关键词

Icariin; nrf2; HO-1; myocardial infarction; inflammatory; immune response

资金

  1. National Key Research and Development Program of China [2018YFA0108700, 2017YFA0105602]
  2. NSFC Projects of International Cooperation and Exchanges [81720108004]
  3. National Natural Science Foundation of China [81974019]
  4. Research Team Project of Natural Science Foundation of Guangdong Province of China [2017A030312007]
  5. key program of Guangzhou science research plan [201904020047]
  6. Special Projects of Dengfeng Program of Guangdong Provincial People's Hospital [DFJH201812, KJ012019119 KJ012020630, KJ012019423]
  7. Natural Science Foundation of China [82001301]
  8. start-up Foundation of Guangdong Province [2018A030310113]
  9. Overseas Famous Teacher Project of Guangdong Provincial Department of Science and Technology [2020A1414010311]
  10. Foundation of Popularization project Department of Inner Mongolia Health commission [202201463]

向作者/读者索取更多资源

Myocardial infarction is a cardiovascular disease caused by problems in the coronary artery. Percutaneous coronary intervention therapy can restore blood perfusion and rescue myocardial cells. Research findings suggest that icariin may prevent cell apoptosis in myocardial infarction by inhibiting proinflammatory factors, making it a potential effective treatment.
Myocardial infarction (MI) is a prevalent cardiovascular disease defined by myocardial ischemia and hypoxic damage caused by plaque rupture, thrombosis, lumen stenosis, or blockage in the coronary artery. However, the development of emergency percutaneous coronary interventional therapy has enabled the rapid restoration of blood perfusion to ischemic myocardium and the rescue of dying myocardium cells. Some dying myocardium cells have caused irreversible damage and impaired cardiac function recovery in recent years. Icariin has been utilized to treat various ailments as a natural chemical extract. In this study, we employed a variety of approaches to observe MI, including western blotting, quantitative RT-PCR, immunohistochemistry, and flow cytometric analysis using icariin. As demonstrated by the research findings, icariin may prevent MI-induced cell apoptosis. This is accomplished by inhibiting proinflammatory factors via the Nrf2/HO-1 signaling pathways. These data imply that icariin may be an effective treatment for MI.

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