Cortistatin Improves Cardiac Function After Acute Myocardial Infarction in Rats by Suppressing Myocardial Apoptosis and Endoplasmic Reticulum Stress

Shi, Zhiyu; Liu, Yue; Li, Dong; Zhang, Bo; Zhao, Meng; Liu, Wenxiu; Zhang, Xin; Yin, Xinhua

doi:10.1177/1074248416644988

Cited by 29 publications

(23 citation statements)

References 35 publications

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“…The results showed that HG combined with hypoxia reduced cell viability and caused cell cycle arrest at G1 phase. ER stress-induced apoptosis contributes to progression of acute MI and anti-apoptotic treatment can reduce infarct size in rats with MI ( 11 ). Our in vitro studies showed that HG combined with hypoxia induced cell apoptosis, activated ER stress and dysregulated ER redox homeostasis, which were consistent with our in vivo results.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that ER stress triggers apoptosis of β cells and results in the onset of diabetes ( 10 ). Additionally, ER stress and myocardial apoptosis are associated with acute MI (AMI) development ( 11 ). Activation of CCAAT/enhancer binding protein (C/EBP)-homologous protein (CHOP) (a marker of ER stress) plays an essential role in ER stress-mediated apoptosis ( 12 ).…”

Section: Introductionmentioning

confidence: 99%

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CCAAT/enhancer binding protein homologous protein knockdown alleviates hypoxia-induced myocardial injury in rat cardiomyocytes exposed to high glucose

Yang

Luo

et al. 2018

Exp Ther Med

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Diabetic patients are more sensitive to ischemic injury than non-diabetics. Endoplasmic reticulum (ER) stress has been reported to be closely associated with the pathophysiology of ischemic injury in diabetes. The aim of the present study was to investigate the mechanisms involved in the progression of diabetes complicated by myocardial infarction (MI) and further verify the role of CCAAT/enhancer binding protein (C/EBP)-homologous protein (CHOP) using an in vitro model of diabetes/MI. The rats were exposed to 65 mg/kg streptozotocin (STZ) and left anterior descending (LAD) coronary artery ligation. ST-segment elevation, heart rate, left ventricular systolic pressure (LVSP) and LV end-diastolic pressure (LVEDP) were measured. Serum creatinine kinase-MB (CK-MB) and cardiac troponin T (cTnT) levels were examined by ELISA. Infarct size and apoptosis were measured by triphenyltetrazolium chloride staining and terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assay. Pathological changes were evaluated by hematoxylin and eosin staining. H9c2 cells were used to establish an in vitro model of diabetes complicated by MI. Following CHOP knockdown, cell viability, cell cycle distribution and apoptosis were examined by Cell Counting Kit-8 assay, flow cytometry and Hoechst staining. Glucose-regulated protein 78 (GRP78), CHOP, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), endoplasmic reticulum oxidoreductase 1 (Ero1)-α, Ero1β and protein disulfide isomerase (PDI) levels in both myocardial tissues and H9c2 cells were determined by western blotting. In the present study, diabetes complicated by MI promoted ST-segment elevation and myocardial apoptosis, increased infarct size, induced pathological changes and elevated LVEDP, CK-MB, cTnT, GRP78, CHOP, Bax, Ero1α, Ero1β and PDI; however, it decreased heart rate, LVSP and Bcl-2. Additionally, high glucose combined with hypoxic treatment reduced cell viability, induced cell cycle arrest at G1 phase, promoted cell apoptosis, and activated the GRP78/CHOP and Ero1/PDI signaling pathways, which were reversed by CHOP knockdown. Thus, CHOP may be an effective therapeutic target for the treatment of diabetes complicated by MI.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

CCAAT/enhancer binding protein homologous protein knockdown alleviates hypoxia-induced myocardial injury in rat cardiomyocytes exposed to high glucose

Yang

Luo

et al. 2018

Exp Ther Med

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“…Acute MI model was established by the permanent ligation of left coronary artery method (Chen et al, 2011;Jin et al, 2015;Shi et al, 2016). Briefly, rats were anesthetized with 10% chloraldurate solution at a dose of 3.8 mL/kg via intraperitoneal (IP) injection, incubated, and ventilated using a respirator pump.…”

Section: Experimental Model Of Acute MImentioning

confidence: 99%

Baicalin-loaded PEGylated lipid nanoparticles: characterization, pharmacokinetics, and protective effects on acute myocardial ischemia in rats

2016

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“…A previous study demonstrated that myocardial ischemia may be the initial factor of ventricular remodeling after AMI (10). Relevant damage-associated stress factors following AMI contribute to regulating myocardial cell death and progression of ventricular remodeling via other approaches (11).…”

Section: Introductionmentioning

confidence: 99%

Ginkgo biloba extract prevents acute myocardial infarction and suppresses the inflammation- and apoptosis-regulating p38 mitogen-activated protein kinases, nuclear factor-κB and B-cell lymphoma 2 signaling pathways

Zhang

Wen

et al. 2017

Molecular Medicine Reports

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Ginkgo biloba is a plant known from the Mesozoic and has been regarded as one of the first to be used in traditional Chinese medicine (TCM). The plant extract has attracted a great deal of attention in recent years. The Ginkgo biloba leaf contains flavones and diterpenes. In addition, Ginkgo biloba performs certain pharmacologic actions, including antioxidant and anti‑aging activities. The aim of the present study was to examine whether Ginkgo biloba extract prevents acute myocardial infarction (AMI). The results demonstrated that Ginkgo biloba extract significantly inhibited infarct size, increased serum histamine levels and weakened creatine kinase (CK)‑MB activity in AMI mice. Ginkgo biloba extract significantly inhibited serum interleukin (IL)‑6 and IL‑1β levels, and caspase‑3/9 activity. In addition, it suppressed matrix metallopeptidase‑9, transforming growth factor‑β, p38 mitogen‑activated protein kinases (MAPK) and nuclear factor (NF)‑κB protein expression, and promoted B‑cell lymphoma 2 (Bcl‑2) protein expression in AMI mice. The results of in vivo assays demonstrated that Ginkgo biloba extract prevents AMI and suppresses inflammation‑ and apoptosis‑regulating p38 MAPK, NF‑κB and Bcl‑2 signaling pathways.

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Cortistatin Improves Cardiac Function After Acute Myocardial Infarction in Rats by Suppressing Myocardial Apoptosis and Endoplasmic Reticulum Stress

Abstract: Exogenous CST has a notable cardioprotective effect after AMI in a rat model in that it improves cardiac function by suppressing ER stress and myocardial apoptosis.

Cited by 29 publications

References 35 publications

CCAAT/enhancer binding protein homologous protein knockdown alleviates hypoxia-induced myocardial injury in rat cardiomyocytes exposed to high glucose

CCAAT/enhancer binding protein homologous protein knockdown alleviates hypoxia-induced myocardial injury in rat cardiomyocytes exposed to high glucose

Baicalin-loaded PEGylated lipid nanoparticles: characterization, pharmacokinetics, and protective effects on acute myocardial ischemia in rats

Ginkgo biloba extract prevents acute myocardial infarction and suppresses the inflammation- and apoptosis-regulating p38 mitogen-activated protein kinases, nuclear factor-κB and B-cell lymphoma 2 signaling pathways

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