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Protective Effect of Geraniol on Oxidative, Inflammatory and Apoptotic Alterations in Isoproterenol-Induced Cardiotoxicity: Role of the Keap1/Nrf2/HO-1 and PI3K/Akt/mTOR Pathways
Antioxidants ( IF 6.0 ) Pub Date : 2020-10-12 , DOI: 10.3390/antiox9100977
Nancy S. Younis , Mohamed S. Abduldaium , Maged E. Mohamed

Background: Myocardial infarction (MI) is still a major contributor to mortality worldwide, and therefore, searching for new drugs is an urgent priority. Natural products are a renewable source for medicinally and pharmacologically active molecules. The objective of this study was to explore the potential of geraniol, a monoterpene alcohol, to protect against MI. Methods: Five groups of Wister rats were used: a control group; a group treated only with geraniol; a group treated only with isoproterenol, to induce MI; and two groups pretreated with geraniol (100 or 200 mg/kg, respectively) for 14 days and challenged with isoproterenol on the 13th and 14th days. Several parameters were measured including electrocardiogram (ECG), cardiac markers, the expression of Kelch-like ECH-associated protein 1 (Keap1), nuclear factor erythroid 2-related factor 2 (Nrf2), and other downstream antioxidant enzymes, as well as the expression of phosphoinositide 3-kinases (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) and other downstream apoptotic and inflammatory mediators. Results: Geraniol treatment reduced the size of the infarct region, attenuated the levels of cardiac indicators, and diminished myocardial necrosis and immune cell infiltration. Geraniol treatment also activated the Keap1/Nrf2/heme oxygenase-1 (HO-1) pathway, increased antioxidant enzyme activities, modulated the PI3K/Akt/mTOR pathway, and ameliorated myocardial autophagy, inflammation, and apoptosis. Conclusion: Geraniol may possess a protective effect against MI through moderating MI-induced myocardial oxidative stress (glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione S-transferase (GST), and Keap1/Nrf2 pathway), inflammation (IL-1β, IL-6, TNF-α, and Nuclear factor-κB (NF-κB)), apoptosis (caspase-3, caspase-9, Bcl2, and Bax), and autophagy (PI3K/Akt/mTOR pathway).

中文翻译:

香叶醇对异丙肾上腺素引起的心脏毒性的氧化,炎症和凋亡变化的保护作用:Keap1 / Nrf2 / HO-1和PI3K / Akt / mTOR途径的作用

背景:心肌梗塞(MI)仍然是导致世界范围内死亡率的主要因素,因此,寻找新药已成为当务之急。天然产物是药物和药理活性分子的可再生来源。这项研究的目的是探索香叶醇(一种单萜醇)预防MI的潜力。方法:使用五组Wister大鼠:对照组;对照组。仅用香叶醇治疗的一组;仅用异丙肾上腺素治疗的组可诱发MI;两组分别用香叶醇(分别为100或200 mg / kg)预处理14天,并在第13天和第14天用异丙肾上腺素攻击。测量了多个参数,包括心电图(ECG),心脏标志物,Kelch样ECH相关蛋白1(Keap1)的表达,核因子红系2相关因子2(Nrf2)和其他下游抗氧化酶,以及磷酸肌醇3激酶(PI3K)/蛋白激酶B(Akt)/雷帕霉素哺乳动物靶标(mTOR)的表达和其他下游凋亡和炎症介质。结果:香叶醇治疗可减少梗塞区域的大小,减弱心脏指标的水平,并减少心肌坏死和免疫细胞浸润。香叶醇的治疗还激活了Keap1 / Nrf2 /血红素加氧酶-1(HO-1)途径,增加了抗氧化酶的活性,调节了PI3K / Akt / mTOR途径,并改善了心肌的自噬,炎症和细胞凋亡。结论:香叶醇可能通过减轻心肌梗死引起的心肌氧化应激(谷胱甘肽(GSH),超氧化物歧化酶(SOD),
更新日期:2020-10-12
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