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《国际心血管病杂志》[ISSN:1006-6977/CN:61-1281/TN]

期数:

2023年04期

页码:

229-234，241

栏目:

基础研究

出版日期:

2023-07-30

文章信息/Info

Title:

Protective effect of salidroside on cardiac function in mice with myocardial infarction?

作者:

刘佳; 武澎; 陈彭生

221009 徐州市中心医院检验科（刘佳）；210029 南京医科大学第一附属医院心内科（武澎）；221009 徐州市中心医院心内科（陈彭生）通信作者：陈彭生，E-mail：wsljxme@163.com

Author(s):

LIU Jia; WU Peng; CHEN Pengsheng

Department of Clinical Laboratory, Xuzhou Central Hospital,Xuzhou 221009

关键词:

红景天苷; 心肌梗死; 心肌重构

Keywords:

Salidroside;  Myocardial infarction;  Myocardial remodeling

分类号:

-

DOI:

10.3969/j.issn.1673-6583.2023.04.010

文献标识码:

-

摘要:

目的：探讨红景天苷（SAL）对心肌梗死小鼠死亡率、心功能和心肌重构的影响。方法：小鼠随机分成假手术（Sham）组、心肌梗死未治疗（MI）组和SAL组，每组小鼠20只，通过结扎小鼠冠状动脉前降支建立小鼠心肌梗死模型，建模后SAL组给予SAL灌胃，MI组和Sham组给予生理盐水灌胃，21后检测各组小鼠的死亡率、心脏功能、心肌纤维化程度和梗死面积及炎症因子表达水平等指标。结果：Sham组、SAL组和MI组的存活率分别为100%、80%和50%（P＜0.05）。与MI组相比，SAL组的心脏质量与体质量比值、肺质

Abstract:

Objective: To investigate whether salidroside (SAL) therapy could reduce mortality, improve cardiac function and alleviate myocardial remodeling in mice with myocardial infarction.? Methods: The mice were divided into Sham group, SAL group and myocardial

参考文献/References

[1]Redfors B, Mohebi RZ, Giustino G, et al. Time delay, infarct size, and microvascular obstruction after primary percutaneous coronary intervention for ST-segment-elevation myocardial infarction[J]. Circ Cardiovasc Interv, 2021, 14(2):e009879.
[2]Ibanez B, James S, Agewall S, et al. 2017 ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation[J]. Kardiol Pol, 2018,76(2):229-313.
[3]Pérez L, Mu?oz-Durango N, Riedel CA, et al. Endothelial-to-mesenchymal transition: cytokine-mediated pathways that determine endothelial fibrosis under inflammatory conditions[J]. Cytokine Growth Factor Rev, 2017, 33:41-54.
[4]Oliveira JB, Soares AASM, Sposito AC. Inflammatory response during myocardial infarction[J]. Adv Clin Chem, 2018, 84:39-79.
[5]Ning W, Li S, Yang W, et al. Blocking exosomal miRNA-153-3p derived from bone marrow mesenchymal stem cells ameliorates hypoxia-induced myocardial and microvascular damage by targeting the ANGPT1-mediated VEGF/PI3k/Akt/eNOS pathway[J]. Cell Signal, 2021, 77:109812.
[6]Bai J, Wang Q, Qi J, et al. Promoting effect of baicalin on nitric oxide production in CMECs via activating the PI3K-AKT-eNOS pathway attenuates myocardial ischemia-reperfusion injury[J]. Phytomedicine, 2019, 63:153035.
[7]Xu F, Xu J, Xiong X, et al. Salidroside inhibits MAPK, NF-κB, and STAT3 pathways in psoriasis-associated oxidative stress via SIRT1 activation[J]. Redox Rep, 2019, 24(1):70-74.
[8]Hu R, Wang MQ, Ni SH, et al. Salidroside ameliorates endothelial inflammation and oxidative stress by regulating the AMPK/NF-κB/NLRP3 signaling pathway in AGEs-induced HUVECs[J]. Eur J Pharmacol, 2020, 867:172797.
[9]Chen L, Liu P, Feng X, et al. Salidroside suppressing LPS-induced myocardial injury by inhibiting ROS-mediated PI3K/Akt/mTOR pathway in vitro and in vivo[J]. J Cell Mol Med, 2017, 21(12):3178-3189.
[10] Gui D, Cui Z, Zhang L, et al. Salidroside attenuates hypoxia-induced pulmonary arterial smooth muscle cell proliferation and apoptosis resistance by upregulating autophagy through the AMPK-mTOR-ULK1 pathway[J]. BMC Pulm Med, 2017, 17(1):191.
[11] Li L, Yang Y, Zhang H, et al. Salidroside ameliorated intermittent hypoxia-aggravated endothelial barrier disruption and atherosclerosis via the cAMP/PKA/RhoA signaling pathway[J]. Front Pharmacol, 2021, 12:723922.
[12] Ni J, Li Y, Xu Y, et al. Salidroside protects against cardiomyocyte apoptosis and ventricular remodeling by AKT/HO-1 signaling pathways in a diabetic cardiomyopathy mouse model[J]. Phytomedicine, 2021, 82:153406.
[13] Schumacher D, Alampour-Rajabi S, Ponomariov V, et al. Cardiac FGF23: new insights into the role and function of FGF23 after acute myocardial infarction[J]. Cardiovasc Pathol, 2019, 40:47-54.
[14] Xu W, Zhang L, Zhang Y, et al. TRAF1 exacerbates myocardial ischemia reperfusion injury via ASK1-JNK/p38 signaling[J]. J Am Heart Assoc, 2019, 8(21):e012575.
[15] Shah DJ, Kim HW, James O, et al. Prevalence of regional myocardial thinning and relationship with myocardial scarring in patients with coronary artery disease[J]. JAMA, 2013, 309(9):909-918.
[16] Li HR, Zheng XM, Liu Y, et al. L-carnitine alleviates the myocardial infarction and left ventricular remodeling through Bax/Bcl-2 signal pathway[J]. Cardiovasc Ther, 2022, 2022:9615674.
[17] Maleszewska M, Moonen JR, Huijkman N, et al. IL-1β and TGFβ2 synergistically induce endothelial to mesenchymal transition in an NFκB-dependent manner[J]. Immunobiology, 2013, 218(4):443-454.
[18] He Z, Opland DM, Way KJ, et al. Regulation of vascular endothelial growth factor expression and vascularization in the myocardium by insulin receptor and PI3K/Akt pathways in insulin resistance and ischemia[J]. Arterioscler Thromb Vasc Biol, 2006, 26(4):787-793.
[19] Yang C, Talukder MA, Varadharaj S, et al. Early ischaemic preconditioning requires Akt- and PKA-mediated activation of eNOS via serine1176 phosphorylation[J]. Cardiovasc Res, 2013, 97(1):33-43.
[20] Zou J, Fei Q, Xiao H, et al. VEGF-A promotes angiogenesis after acute myocardial infarction through increasing ROS production and enhancing ER stress-mediated autophagy[J]. J Cell Physiol, 2019, 234(10):17690-17703.

备注/Memo

备注/Memo:

基金项目：国家自然科学基金（82000335）；徐州市科技项目（KC17125）
（收稿：2022-08-15 修回：2023-04-02）

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更新日期/Last Update: 2023-08-01