Inflammatory Mechanisms and Treatment of Myocardial Infarction | ||||
| Records of Pharmaceutical and Biomedical Sciences | ||||
| Article 15, Volume 6, Issue 3, April 2022, Page 172-178 PDF (577.8 K) | ||||
| Document Type: Mini-reviews | ||||
| DOI: 10.21608/rpbs.2022.162152.1169 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
Abdelrahman Mahmoud Rizk  1; Mona Farag El-Azab 2; Reem Hazem 3; Heba Abdelrazek4
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| 1Clinical pharmacist, Suez canal authority | ||||
| 2Department of Pharmacology and Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia, Egypt | ||||
| 3Pharmacology & toxicology Department, Faculty of Pharmacy, Suez Canal University, Ismailia, 41522, Egypt. | ||||
| 4Professor of Physiology Faculty of Veterinary Medicine Suez Canal University | ||||
| Abstract | ||||
| Myocardial infarction (MI) is the one of the most severe manifestations of coronary artery disease which may lead to severe complications as heart failure. MI is also still an important cause of death in both developed and western countries. One of the most crucial mechanisms causing MI induced complications is inflammasome activation and subsequent release of inflammatory cytokines. A significant rise in cardiac enzymes troponin I and creatine kinase-MB (CK-MB) was observed, also significant rise in inflammatory markers interleukin 1β (IL-1β) serum levels, toll like receptor 4 (TLR4) and NF-κB were observed in MI. Moreover, increase in the expression of all inflammasome components as NLRP3 and caspase-1 was detected along with histopathological and electrocardiographic abnormalities as changes in ST segment elevation and QT interval prolongation. The current study shows that targeting the inflammatory cascade through inhibiting one of its important activators the inflammasome may be a novel strategy for management of MI and preventing its complications. | ||||
| Keywords | ||||
| Inflammasome; NF-κB; Myocardial infarction | ||||
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