ATP-Sensitive Potassium Channels Mediate the Cardioprotective Effect of Panax notoginseng Saponins against Myocardial Ischaemia–Reperfusion Injury and Inflammatory Reaction

التفاصيل البيبلوغرافية
العنوان: ATP-Sensitive Potassium Channels Mediate the Cardioprotective Effect of Panax notoginseng Saponins against Myocardial Ischaemia–Reperfusion Injury and Inflammatory Reaction
المؤلفون: Yi-Min Bao, Ting Hu, Xingyu Wang, Ai-Hua Liu, Ke Ning, Li Jiang
المصدر: BioMed Research International, Vol 2020 (2020)
بيانات النشر: Hindawi Limited, 2020.
سنة النشر: 2020
مصطلحات موضوعية: 0301 basic medicine, Cardiac function curve, endocrine system, Article Subject, Ischemia, Inflammation, 030204 cardiovascular system & hematology, Pharmacology, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, 0302 clinical medicine, medicine, Panax notoginseng, Nicorandil, General Immunology and Microbiology, biology, business.industry, Inflammasome, General Medicine, medicine.disease, biology.organism_classification, Potassium channel, 030104 developmental biology, Medicine, medicine.symptom, business, Reperfusion injury, hormones, hormone substitutes, and hormone antagonists, medicine.drug
الوصف: Inflammatory response during myocardial ischemia reperfusion injury (MIRI) is essential for cardiac healing, while excessive inflammation extends the infarction and promotes adverse cardiac remodeling. Understanding the mechanism of these uncontrolled inflammatory processes has a significant impact during the MIRI therapy. Here, we found a critical role of ATP-sensitive potassium channels (KATP) in the inflammatory response of MIRI and its potential mechanism and explored the effects of Panax Notoginseng Saponins (PNS) during this possess. Rats underwent 40 min ischemia by occlusion of the left anterior descending (LAD) coronary artery and 60 min of reperfusion. PNS was treated at the corresponding time point before operation; 5-hydroxydecanoate (5-HD) and glybenclamide (Gly) (or Nicorandil (Nic)) were used as pharmacological blocker (or nonselective opener) of KATP. Cardiac function and pathomorphology were evaluated and a set of molecular signaling experiments was tested. KATP current density was measured by patch-clamp. Results revealed that in MIRI, PNS pretreatment restored cardiac function, reduced infarct size, and ameliorated inflammation through KATP. However, inhibiting KATP by 5-HD and Gly significantly reversed the effects, including NLRP3 inflammasome and inflammatory mediators IL-6, MPO, TNF-α, and MCP-1. Moreover, PNS inhibited the phosphorylation and nuclear translocation of NF-κB in I/R myocardium when the KATP was activated. Importantly, PNS promoted the expression of subunits and activation of KATP. The study uncovered KATP served as a new potential mechanism during PNS modulating MIRI-induced inflammation and promoting injured heart recovery. The manipulation of KATP could be a potential therapeutic approach for MIRI and other inflammatory diseases.
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تدمد: 2314-6141
2314-6133
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c127ea4f3ff30bbcb3fb344cd793662c
https://doi.org/10.1155/2020/3039184
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....c127ea4f3ff30bbcb3fb344cd793662c
قاعدة البيانات: OpenAIRE