Expression of inflammatory and apoptosis factors following coronary stent implantation in coronary heart disease patients

Liu, Li‐Li; Lin, Li‐Rong; Lu, Chengxiang; Fu, Jianguo; Chao, Peng-Li; Jin, Hongwei; Zhang, Zhongying

doi:10.1016/j.intimp.2011.07.015

Cited by 6 publications

(9 citation statements)

References 18 publications

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“…Prospective review and randomized clinical trials have investigated factors associated with increased coronary heart disease risk ( 31 ). Expression of apoptosis factors following coronary heart disease are increased in patients in the clinic ( 32 ). Data in a systematic review and meta-analysis indicate the therapeutic effects of perioperative statins on death, myocardial infarction, atrial fibrillation and length of stay ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

Statin rosuvastatin inhibits apoptosis of human coronary artery endothelial cells through upregulation of the JAK2/STAT3 signaling pathway

Wang¹,

Li²,

Xie³

et al. 2020

Mol Med Rep

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The purpose of the present study was to explore the potential molecular signaling pathway mediated by the statin rosuvastatin in cultured human coronary artery endothelial cells (Hcaecs) induced by cocl 2. cocl 2 was used to induce the apoptosis of Hcaecs. Myocardial infarction rats were established and received statin or PBS treatment. reverse transcription-quantitative Pcr, western blotting, eliSa, Tunel assay and immunohistochemistry were used to analyze the role of statin treatment. The results showed that rosuvastatin treatment decreased apoptosis of Hcaecs induced by cocl 2 by increasing anti-apoptosis Bcl-xl and Bcl-2 expression, and decreasing pro-apoptosis Bax, Bad, caspase-3 and caspase-9 expression. The myocardial ischemia rat model demonstrated that rosuvastatin treatment decreased the mitochondrial reactive oxygen species, inflammation, mitochondrial damage, lipid catabolism, heart failure and the myocardial infarction areas, but improved the cardiac function indicators, right and left ventricular ejection fraction and increased expression levels of Janus kinase (JaK) and signal transducer and activator of transcription (STaT)3 in myocardial tissue. in conclusion, the results of the current study revealed that the statin rosuvastatin presents cardioprotective effects by activation of the JaK2/STaT3 signaling pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Statin rosuvastatin inhibits apoptosis of human coronary artery endothelial cells through upregulation of the JAK2/STAT3 signaling pathway

Wang¹,

Li²,

Xie³

et al. 2020

Mol Med Rep

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show abstract

“…Previous studies have indicated that apoptosis of cardiomyocytes is crucial in cardiac dysfunction following acute myocardial infarction in the development of coronary heart disease ( 39 , 40 ). Numerous strategies aimed at preventing or mitigating the extent of apoptosis have been attempted to protect the heart against coronary heart disease-induce apoptosis or death of cardiomyocytes ( 41 – 43 ). In the current study, prazosin treatment significantly inhibited apoptosis of myocardial cells by upregulation of Bcl-2 and p53, as well as downregulation of caspase-3, caspase-9, Bcl-2 and p53 in myocardial cells in a mouse model of anoxia-reoxygenation injury.…”

Section: Discussionmentioning

confidence: 99%

Prazosin protects myocardial cells against anoxia-reoxygenation injury via the extracellular signal‑regulated kinase signaling pathway

Wang

Xue

et al. 2017

Mol Med Report

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Ischemic heart disease (including coronary arterial atherosclerosis, or vascular cavity stenosis or occlusion) remains the leading cause of disease-associated mortality worldwide. Prazosin, a receptor blocker of postsynaptic adrenaline, is essential in expanding peripheral arteries, which decreases peripheral vascular resistance, and regulates anti-hypertensive action. However, the mechanisms underlying the effects of prazosin have not been fully elucidated. The aim of the present study was to investigate the protective effects of prazosin on myocardial cells against anoxia-reoxygenation injury in a mouse model. The regulatory effects of prazosin on blood lipid levels and blood pressure were investigated in experimental mice. Furthermore, inflammation responses and oxidative stress in myocardial cells were analyzed in mice treated with prazosin. Apoptotic myocardial cells were investigated in experimental mice treated with prazosin. In addition, apoptotic gene expression levels were evaluated in myocardial cells. Extracellular signal-regulated kinase (ERK) expression and phosphorylation was investigated in myocardial cells in mice with anoxia-reoxygenation injury following prazosin treatment. The activity and expression levels of nuclear factor of activated T cells (NF-AT), activator protein 1 (AP-1) and necrosis factor (NF)-κB were observed in myocardial cells. Furthermore, histological analyses were performed to investigate the benefits of prazosin treatment on anoxia-reoxygenation injury. The results of the present study identified that prazosin decreased the expression levels of inflammatory factors, interleukin (IL)-6, tumor necrosis factor (TNF)-α, IL-10 and IL-1 in the serum of mice exhibiting hypoxia/reoxygenation injury. Oxidative stress was observed to be improved and the apoptosis rate was decreased in myocardial cells in anoxia-reoxygenation injury model mice treated with prazosin. ERK expression and phosphorylation was upregulated, and expression levels of NF-AT, AP-1 and NF-κB were downregulated in the myocardial cells of mice treated with prazosin. Blood lipid levels and blood pressure of the anoxia-reoxygenation injury model mice were markedly improved following treatment with prazosin. Histological analysis indicated that the area, circumference fragmentation and segmentation of myocardial cells were significantly improved following prazosin treatment. Thus, these results indicate that prazosin treatment decreases inflammation responses, oxidative stress, and apoptosis of myocardial cells via regulation of the ERK signaling pathway. The findings indicate that prazosin may present as a potential therapeutic agent for the treatment of hypoxia/reoxygenation injury.

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“…Furthermore, it has been demonstrated that berberine inhibits ischemia-induced apoptosis by activating the PI3K/PKB signaling pathway (22). Therefore, various strategies aiming at preventing or mitigating the extent of apoptosis have been performed to try to protect the small intestine against apoptosis or necrosis (23,27,28). In the present study, it was hypothesized that berberine may regulate the apoptosis of epithelial cells in a mouse model of neonatal NEC by regulating the PI3K/AKT signaling pathway.…”

Section: Discussionmentioning

confidence: 88%

“…Previous studies have reported that preventing inflammation is an effective method of protecting against myocardial ischemia-reperfusion injury and have highlighted it as a novel technique of diagnosing and treating patients with cardiac disease (23,24). Loubele et al (24) reported that the inhibition of apoptosis and inflammation contributes to the rehabilitation of myocardial ischemia/reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

Berberine ameliorates neonatal necrotizing enterocolitis by activating the phosphoinositide 3-kinase/protein kinase B signaling pathway

et al. 2018

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Expression of inflammatory and apoptosis factors following coronary stent implantation in coronary heart disease patients

Cited by 6 publications

References 18 publications

Statin rosuvastatin inhibits apoptosis of human coronary artery endothelial cells through upregulation of the JAK2/STAT3 signaling pathway

Statin rosuvastatin inhibits apoptosis of human coronary artery endothelial cells through upregulation of the JAK2/STAT3 signaling pathway

Prazosin protects myocardial cells against anoxia-reoxygenation injury via the extracellular signal‑regulated kinase signaling pathway

Berberine ameliorates neonatal necrotizing enterocolitis by activating the phosphoinositide 3-kinase/protein kinase B signaling pathway

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