ReferenceID 2992
Anethole's effects against myocardial infarction: The role of TLR4/NFκB and Nrf2/HO1 pathways
Chem Biol Interact
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 medi
Relationship Network
Interactive first-hop connections across herbs, ingredients, formulas, targets, diseases, symptoms, syndromes, evidence, and monographs.
Click a node to open it in a new tab
Ingredient: 1Reference: 1Links: 1
Arranging relationship network...
Record Fields
Scalar fields from the final reference record.
- Reference Id
- 2992
- Evidence Id
- 19582
- Core Evidence Id
- 19582
- Source Reference Id
- 5993
- Herb2 Reference Id
- HBREF006790
- Subject Paper Key
- HBIN046713_35430261
- Pubmed Id
- 35430261
- Doi
- 10.1016/j.cbi.2022.109947
- Paper Title
- Anethole's effects against myocardial infarction: The role of TLR4/NFκB and Nrf2/HO1 pathways
- Paper 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.
- Journal
- Chem Biol Interact
- Publish Year
- 2022
- Experiment Subject
- rat
- Experiment Type
- Animal Experiment
- Phenotype Related
- Myocardial Inflammation; Myocardial Infarction; Myocardial Necrosis
- Paper Title Cn
- Paper Title En
- Anethole's effects against myocardial infarction: The role of TLR4/NFκB and Nrf2/HO1 pathways
- Bilingual Status
- semi_complete