Anethole's effects against myocardial infarction: The role of TLR4/NFκB and Nrf2/HO1 pathways. (1st June 2022)

• Record Type: Journal Article
• Authors: Younis, Nancy S.; Mohamed, Maged E.
• Is Part Of: Chemico-biological interactions. Volume 360(2022)
• Publication Date: 2022-06-01
• Subjects: Anethole -- Apoptosis -- Essential oil -- Inflammatory mediators -- Myocardial infarction -- Oxidative stress; Biochemistry -- Periodicals; Toxicological chemistry -- Periodicals; Biochemistry -- Periodicals; Biologie moléculaire -- Périodiques; Biochimie -- Périodiques; Toxicologie biochimique -- Périodiques; 572
• DOI: 10.1016/j.cbi.2022.109947
• Languages: English
• ISSNs: 0009-2797

Abstract

Abstract: Background: Exploring new drugs for the management of myocardial infarction (MI) is crucial, as MI is a major contributor to mortality worldwide. Anethole, a naturally occurring essential oil component, has numerous medicinal, pharmaceutical, and cosmetic purposes. This study explored the potential action of anethole to protect myocytes against MI injure. Methods: Wistar rats were divided into five groups: normal; anethole; and isoproterenol (ISO) groups in addition to two groups of ISO + anethole (125 and 250 mg/kg). All anethole groups were administered the oil component for 30 days, and all ISO groups were challenged with ISO on the 28th and 29th days. Parameters measured included infracted area, ECG, cardiac markers, the expression of Keap 1, nuclear Nrf2, and heme oxygenase-1, as well as the expression of TLR4 and MYD88 together with subsequent downstream oxidative stress, inflammatory, and apoptotic markers. Results: Anethole reduced infarct region, degenerated cardiac indicators levels, amended ECG alterations, and diminished myocardial necrosis. Anethole reduced Keap-1, activated Nrf2/HO-1 pathway, increased mitochondrial antioxidant enzyme activities, declined the TLR4/MYD88 pathway, and ameliorated myocardial inflammation and cell death markers. Conclusion: Anethole may retain a cardio-protective potential by controlling myocardial oxidative stress (through Nrf2 pathway) and diminishing inflammation and apoptosis via the TLR4/MYD88 pathway. Highlights: Anethole, protects against ISO-induced myocardial infarction insult. Anethole inhibits MYD88/TLR4, inflammation and apoptosis. Anethole triggers the Keap1/Nrf2/HO-1 pathway. Anethole protected heart from the oxidative stress and inflammation.