Zaafan Mai A, Abdelhamid Amr M
Pharmacology and Toxicology Department, Faculty of Pharmacy, October University for Modern Sciences and Arts (MSA), Egypt.
Biochemistry Department, Faculty of Pharmacy, October University for Modern Sciences and Arts (MSA), Egypt.
Noncoding RNA Res. 2024 Sep 10;10:192-197. doi: 10.1016/j.ncrna.2024.09.007. eCollection 2025 Feb.
Globally, myocardial infarction (MI) is one of the main causes of death. This study aims to investigate the role of miR-217 in the pathogenesis through targeting MAPK and PI3K/AKT signaling pathways in experimental model of myocardial infarction and studying the possible cardioprotective role of dihydromyricetin (DHM) through modulation of this pathway.
Dihydromyricetin was injected (100 mg/kg; p.o.) in isoprenaline induced myocardial infarction rat model for 14 days. Rats were anaesthetized and blood samples were taken for serum separation, estimation of creatine kinase-MB (CK-MB), and troponin-I levels after 24 h had passed since the last isoprenaline injection. In addition, the hearts were also used for the other biochemical studies and the histological evaluation.
DHM resulted in a significant suppression of the elevated levels miR-217 and MAPK compared to the MI control group and restored the normal level of serum CK-MB. Furthermore, DHM successfully restored the oxidative balance and halted the pro-inflammatory mediators in the cardiac tissue.
Accordingly, our experiment emphasizes the anti-ischemic property that has been demonstrated through modulation of expression level of miR-217 and consequent deactivation of MAPK and PI3K/AKT signaling pathways, and this was assured by halting downstream pro-inflammatory markers.
在全球范围内，心肌梗死（MI）是主要的死亡原因之一。本研究旨在通过在心肌梗死实验模型中靶向丝裂原活化蛋白激酶（MAPK）和磷脂酰肌醇-3激酶/蛋白激酶B（PI3K/AKT）信号通路来研究miR-217在发病机制中的作用，并通过调节该通路研究二氢杨梅素（DHM）可能的心脏保护作用。
在异丙肾上腺素诱导的心肌梗死大鼠模型中注射二氢杨梅素（100mg/kg；口服），持续14天。大鼠麻醉后，自最后一次注射异丙肾上腺素24小时后采集血样进行血清分离，测定肌酸激酶同工酶MB（CK-MB）和肌钙蛋白I水平。此外，心脏还用于其他生化研究和组织学评估。
与心肌梗死对照组相比，二氢杨梅素导致miR-217和MAPK升高水平显著降低，并使血清CK-MB恢复正常水平。此外，二氢杨梅素成功恢复了氧化平衡并阻止了心脏组织中的促炎介质。
因此，我们的实验强调了通过调节miR-217表达水平以及随后使MAPK和PI3K/AKT信号通路失活所证明的抗缺血特性，这通过阻止下游促炎标志物得以证实。
