Protective effects of myrrh essential oil on isoproterenol-induced myocardial infarction in rats through antioxidant, anti-inflammatory, Nrf2/HO-1 and apoptotic pathways

生理盐水 传统医学 抗氧化剂 医学 氧化应激 精油 脂质过氧化 药理学 心肌梗塞 内分泌学 内科学 化学 食品科学 生物化学
作者
Nancy S. Younis,Maged E. Mohamed
出处
期刊:Journal of Ethnopharmacology [Elsevier BV]
卷期号:270: 113793-113793 被引量:29
标识
DOI:10.1016/j.jep.2021.113793
摘要

Myrrh, a traditional remedy, is the stem resinous exudate of Commiphora molmol Engler (Burseraceae). The aromatic yellowish-brown oleoresin has a long history in folk and traditional medicine, in Saudi Arabia and the Arab world. Severe universal concern attributable to the high mortality is Myocardial Infarction (MI). Acute administration of Isoproterenol (ISO) is an established animal model to induce myocardial injury. The existing animal study was outlined to inspect the actions of Myrrh essential oil on cardiac functional, antioxidant status, apoptotic and inflammatory deviations in isoproterenol induced MI. Normal and Myrrh control animals were administered normal saline and Myrrh essential oil for thirty days orally, respectively. On the 29th and 30th day, the animals were injected by saline (s.c.). In the ISO control, the animals were administered saline orally for 30 days and then confronted with ISO (85 mg/kg s.c.) on 29th and 30th days. In the Myrrh Groups (IV and V), the animals were treated with Myrrh essential oil (50 and 100 mg/k) respectively for 30 days and injected with ISO (85 mg/kg, s.c.) on 29th and 30th days. Animals experienced MI displayed functional blood pressure deviations, intensification in the heart to body weight ratio, myocytes indicative markers (CK-MB, CPK, LDH, cTnT, cTnI), lipid peroxidation (MDA), protein expression of Nrf2 and HO-1, apoptotic markers (Caspase 3,9), and inflammatory indicators. Conversely, animals pre-treated with Myrrh revealed obliteration of those elevations triggered by ISO induction, diminished elevated biochemical values and improved heart function. Conclusion: Myrrh abstain effective cardio-protective action in MI model through improving the oxidative condition with myocytes and abolishing apoptotic as well as inflammatory responses.
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