Annexin A3 gene silencing promotes myocardial cell repair through activation of the PI3K/Akt signaling pathway in rats with acute myocardial infarction

Abstract Background Araloside C (AsC), a natural saponin isolated from Aralia elata, has a wide range of anti-inflammatory properties and has been found in recent years to have heart-protective effects. Present study aimed to determine the effects of AsC on myocardial cell apoptosis through regulating PI3K/AKt. Methods and Results Statistical analyses were performed using GraphPadPrism7.0 software. The differences between two groups and multiple groups were analyzed using t-test and one-way ANOVA, respectively. In vivo results showed that AsC administration could improve cardiac functions and apoptotic rate in HF model through PI3K/AKt signaling pathway, including increasing left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS), and decreasing left ventricular end systolic diameter (LVESD) and left ventricular end diastolic diameter (LVEDD) in detection of myocardial function, inhibiting LDH, CK, CK-MB, CK and HBDH in biochemical index level assessment, inhibiting BNP, ANG II, IL-1b, IL-4, IL-6 and TNF-a in immunological index level. ASC regulates the expression of key apoptotic molecules, including increasing the expression of Bcl-2 and Bax. ASC also regulates phosphorylation of p-PI3K and p-Akt.Conclusion This study suggested for the first time that AsC could partially regulate the PI3K/AKt signaling pathway to prevent myocardial cell apoptosis. This study provided a basis for further research on effective substances in the treatment of HF.

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Extracellular vesicles derived from myocardial infarction plasma inhibit BMSCs apoptosis and enhance cardiac function via AKT signaling pathway

International Immunopharmacology ◽

10.1016/j.intimp.2021.107730 ◽

2021 ◽

Vol 96 ◽

pp. 107730

Author(s):

Peifeng Jin ◽

Lu Ding ◽

Lei Wang ◽

Sheng Jiang ◽

Jiakan Weng ◽

...

Keyword(s):

Myocardial Infarction ◽

Cardiac Function ◽

Signaling Pathway ◽

Extracellular Vesicles ◽

Akt Signaling ◽

Akt Signaling Pathway

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Rian/miR-210-3p/Nfkb1 feedback loop promotes hypoxia-induced cell apoptosis in myocardial infarction via deactivating PI3K/Akt signaling pathway

Journal of Cardiovascular Pharmacology ◽

10.1097/fjc.0000000000000824 ◽

2020 ◽

Vol Publish Ahead of Print ◽

Author(s):

Lihua Zhong ◽

Jing Jia ◽

Guohui Ye

Keyword(s):

Myocardial Infarction ◽

Signaling Pathway ◽

Cell Apoptosis ◽

Feedback Loop ◽

Akt Signaling ◽

Akt Signaling Pathway

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Thyroid hormone mediates cardioprotection against postinfarction remodeling and dysfunction through the IGF-1/PI3K/AKT signaling pathway

10.21203/rs.3.rs-22987/v1 ◽

2020 ◽

Author(s):

Bin Zeng ◽

Xiaoting Liao ◽

Lei Liu ◽

Caixia Zhang ◽

Huaiyu Ruan

Keyword(s):

Myocardial Infarction ◽

Cardiovascular Diseases ◽

Thyroid Hormone ◽

Signaling Pathway ◽

Akt Signaling ◽

Left Ventricular ◽

Sham Operation ◽

Akt Signaling Pathway ◽

Anti Inflammatory ◽

Related Proteins

Abstract Background Severe cardiovascular diseases, such as myocardial infarction or heart failure, can alter thyroid hormone (TH) secretion and peripheral conversion, leading to low triiodothyronine (T3) syndrome. Accumulating evidence suggests that TH has protective properties against cardiovascular diseases and that treatment with TH can effectively reduce myocardial damage after myocardial infarction (MI). However, the potential mechanisms are not clear. This study was designed to investigate the effect of T3 pretreatment on cardiac function and pathological changes in mice subjected to MI and the underlying mechanisms. Methods Adult male C57BL/6 mice underwent surgical ligation of the left anterior descending coronary artery (LAD) (or sham operation) to establish a myocardial infarction model. T3, BMS-754807 (inhibitor of insulin-like growth factor-1 receptor (IGF-1R)) or vehicle was administered before surgery. Results Compared with the MI group, the T3 pretreatment group exhibited significant attenuation of the myocardial infarct area, inhibition of cardiomyocyte apoptosis and fibrosis, and improved left ventricular function after MI. In addition, T3 exhibited an enhanced potency to stimulate angiogenesis and exert anti-inflammatory effects by reducing the levels of serum inflammatory cytokines after myocardial infarction. However, all of these protective effects were inhibited by the IGF-1R inhibitor BMS-754807. Moreover, the protein expression of IGF-1/PI3K/AKT signaling-related proteins, such as IGF-1, IGF-1R, phosphorylated PI3K (p-PI3K) and p-AKT was significantly upregulated in MI mice that received T3 pretreatment, and BMS-754807 pretreatment blocked the upregulation of the expression of these signaling-related proteins. Conclusion T3 pretreatment can protect the heart against dysfunction post-MI through its anti-apoptotic, anti-fibrotic, anti-inflammatory and angiogenesis-stimulating effects, which may be mediated by the activation of the IGF-1/PI3K/AKT signaling pathway.

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