The cardioprotective effects of acteoside in myocardial ischemia reperfusion injury and the underlying mechanism.

IF 2 3区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS
Jing Li, Yuxin Guo, Yang Yang, Qing Xue, Hong Cao, Guangyuan Yang, Zhiqi Sun, Lin-Lin Jia, Hai-Bo Yu
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引用次数: 0

Abstract

Introduction: We observed the cardioprotective effects of Acteoside (AC) on myocardial ischemia reperfusion injury (MIRI) and discussed the possible mechanisms.

Methods: Before MIRI model was established successfully, AC was administrated to SD rats by gastric route for 7 d. Punctuate paw withdrawal threshold (PWT) was recorded to reflect the pain threshold. Blood samples were collected to measure the levels of oxidative stress, myocardial enzymes and Norepinephrine (NE). Hematoxylin and eosin (HE) staining was performed to observe the pathological changes of myocardial tissues. Apoptosis of myocardial cell was determined by transferase-mediated dUTP nick end labeling (TUNEL) assay, and the expressions of Bcl-2 and Bax were determined by Western blotting. Using network pharmacological analysis, the PI3K/Akt signaling pathway was screened to be associated with both AC and MIRI. Subsequently, the expressions of PI3K, p-Akt and caspase-3 were detected by immunochemistry in myocardial tissues.

Results: We found that pre-administration of AC improved pain threshold and pathological change of myocardial structure caused by MIRI. AC reduced serum levels of myocardial enzymes and NE in MIRI. Compared with the Sham group, rats in MIRI group showed enhanced oxidative stress levels. These changes were partly reversed by AC. In addition, AC inhibited apoptosis, regulated the expression of apoptosis-related proteins. Immunochemistry analysis confirmed that AC increased the expressions of PI3K and p-Akt in myocardial tissue.

Conclusion: The cardioprotective effects of AC in MIRI were related with pain alleviation, oxidative stress, apoptosis and sympathetic nerve activity inhibition, the PI3K/Akt signal pathway activation.

Clinical trial number: Not applicable.

毛蕊花苷对心肌缺血再灌注损伤的保护作用及其机制。
前言:我们观察了毛蕊花苷(AC)对心肌缺血再灌注损伤(MIRI)的保护作用,并探讨了其可能的机制。方法:在成功建立MIRI模型前,SD大鼠经胃路给药AC 7 d,记录间断爪戒断阈值(PWT),反映疼痛阈值。采集血液样本,测定氧化应激、心肌酶和去甲肾上腺素(NE)水平。采用苏木精、伊红(HE)染色观察大鼠心肌组织的病理变化。采用转移酶介导dUTP缺口末端标记法(TUNEL)检测心肌细胞凋亡,Western blotting检测Bcl-2、Bax的表达。通过网络药理学分析,我们筛选出PI3K/Akt信号通路与AC和MIRI均相关。免疫化学法检测心肌组织中PI3K、p-Akt和caspase-3的表达。结果:我们发现预给药可改善MIRI引起的痛阈和心肌结构的病理改变。AC降低了MIRI患者心肌酶和NE的血清水平。与Sham组比较,MIRI组大鼠氧化应激水平升高。AC可部分逆转这些变化。此外,AC可抑制细胞凋亡,调节细胞凋亡相关蛋白的表达。免疫化学分析证实AC增加了心肌组织中PI3K和p-Akt的表达。结论:AC对MIRI的心脏保护作用与缓解疼痛、氧化应激、细胞凋亡、抑制交感神经活动、激活PI3K/Akt信号通路有关。临床试验号:不适用。
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来源期刊
BMC Cardiovascular Disorders
BMC Cardiovascular Disorders CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
3.50
自引率
0.00%
发文量
480
审稿时长
1 months
期刊介绍: BMC Cardiovascular Disorders is an open access, peer-reviewed journal that considers articles on all aspects of the prevention, diagnosis and management of disorders of the heart and circulatory system, as well as related molecular and cell biology, genetics, pathophysiology, epidemiology, and controlled trials.
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