Effect of Diazoxide Preconditioning on Cultured Rat Myocardium Microvascular Endothelial Cells against Apoptosis and Relation of PI3K/Akt Pathway

Cao, Sheng‐Li; Xia, Tao; Ren, Shengxiang; Qing, She; Jing, Ding; Huang, Lian; Qin, Bin; Yuan, Zhiwen; Zhu, Xiaohui

doi:10.5152/balkanmedj.2013.8458

Cited by 8 publications

(3 citation statements)

References 10 publications

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“…A previous study revealed that PI3K-AKT signaling inhibited human cardiac microvascular endothelial cells (HCMEC) apoptosis and hypoxia/reoxygenation (HR)-induced endothelial dysfunction. Moreover, the PI3K-AKT pathway prevented HR-induced myocardial microvascular endothelial cell apoptosis (Su et al, 2014). Increased levels of Bcl-2, PI3K, and phosphorylated AKT can protect HCMECs from HR injury (Xie et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

A glucagon-like peptide-1 analog, liraglutide, ameliorates endothelial dysfunction through miRNAs to inhibit apoptosis in rats

Zhang¹,

Xiao²,

Zheng³

et al. 2019

PeerJ

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Background and Aims Many studies have revealed that glucagon-like peptide-1 has vasoprotective effects. In this study, we investigated whether liraglutide suppressed endothelial dysfunction and explored the mechanism involved. Methods Experimental diabetes was induced through combined high-fat diet administration and intraperitoneal streptozotocin injections. Rats were randomly divided into the following four groups: control, diabetes, diabetes + a low liraglutide dose (0.2 mg/kg/d), and diabetes + a high liraglutide dose (0.4 mg/kg/d). Endothelial function and metabolic parameters were measured after 8 weeks of treatment. miRNA arrays were analyzed to identify the differentially expressed miRNAs. Results We found that liraglutide significantly improved aortic endothelial function in diabetic rats. Liraglutide inhibited miR-93-5p, miR-181a-5p and miR-34a-5p expression, and activated miR-26a-5p expression. miRNA mimic transfection experiments indicated negative relationships between miR-93-5p, miR-181a-5p, miR-34a-5p, and miR-26a-5p and Sirt1, Creb, Bcl-2, and Pten expression, respectively. Moreover, liraglutide increased Sirt1, Creb, and Bcl-2 expression levels and reduced Pten expression level. Conclusion Our results demonstrate the role of key miRNAs in the liraglutide-mediated regulation of endothelial cell function in diabetic rats.

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Section: Discussionmentioning

confidence: 99%

A glucagon-like peptide-1 analog, liraglutide, ameliorates endothelial dysfunction through miRNAs to inhibit apoptosis in rats

Zhang¹,

Xiao²,

Zheng³

et al. 2019

PeerJ

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show abstract

“…The anti-inflammatory effects of GLP-1RA liraglutide -via NF-kB downregulation and reduced synthesis of inflammatory cytokines (MCP-1, TNFα, INF-γ and IL-6)- and the concomitant eNOS activation suggest its protective vascular effects, irrespective of glucose-lowering activity [200]. Indeed, liraglutide beneficial effects on vascular function have been linked to downregulated expression of 12 miRNAs including miR-93-5p, miR-181a-5p and miR-34a-5p and upregulated levels of 33 miRNAs including miR-26a-5p [201].…”

Section: Epigenetic Modifications Induced By Standard Anti-hyperglmentioning

confidence: 99%

Can Epigenetics of Endothelial Dysfunction Represent the Key to Precision Medicine in Type 2 Diabetes Mellitus?

Coco

Sgarra

Potenza

et al. 2019

IJMS

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In both developing and industrialized Countries, the growing prevalence of Type 2 Diabetes Mellitus (T2DM) and the severity of its related complications make T2DM one of the most challenging metabolic diseases worldwide. The close relationship between genetic and environmental factors suggests that eating habits and unhealthy lifestyles may significantly affect metabolic pathways, resulting in dynamic modifications of chromatin-associated proteins and homeostatic transcriptional responses involved in the progression of T2DM. Epigenetic mechanisms may be implicated in the complex processes linking environmental factors to genetic predisposition to metabolic disturbances, leading to obesity and type 2 diabetes mellitus (T2DM). Endothelial dysfunction represents an earlier marker and an important player in the development of this disease. Dysregulation of the endothelial ability to produce and release vasoactive mediators is recognized as the initial feature of impaired vascular activity under obesity and other insulin resistance conditions and undoubtedly concurs to the accelerated progression of atherosclerotic lesions and overall cardiovascular risk in T2DM patients. This review aims to summarize the most current knowledge regarding the involvement of epigenetic changes associated with endothelial dysfunction in T2DM, in order to identify potential targets that might contribute to pursuing “precision medicine” in the context of diabetic illness.

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“…The PI3K/Akt signaling pathway is involved in the regulation of cells survival and apoptosis, and is regarded to be a potential neuroprotective mechanism (Xu et al, 2021). Specifically, when Akt was activated by phosphorylated PI3K, it would translocate to the nucleus or cytoplasm after detached from the cell membrane, and further regulated apoptosis signals (Su et al, 2014). Akt can directly bind to pro‐apoptosis proteins (e.g., Bax) and inhibit these expressions, and promote the expression of anti‐apoptosis proteins (e.g., Bcl‐2).…”

Section: Discussionmentioning

confidence: 99%

Lutein attenuated methylglyoxal‐induced oxidative damage and apoptosis in PC12 cells via the PI3K /Akt signaling pathway

Chen

Zhang

Liu

et al. 2022

Journal of Food Biochemistry

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Methylglyoxal (MGO), a cytotoxic byproduct of glycolysis, causes neuro oxidative damage and apoptosis, and plays key roles in diabetic encephalopathy (DE). The goal of this research was to evaluate the roles of lutein attenuated MGO‐induced damage in PC12 cells as well as the underlying mechanisms. The findings of this study showed that lutein has a significant impact on reducing the generation of reactive oxygen species (ROS) and oxidative stress in MGO‐induced PC12 cells, which may be attributed to the increased antioxidant enzymes activity and the decreased MDA levels. Moreover, treatment with lutein also alleviated cell apoptosis and mitochondrial damage. Real‐time PCR and western blot analysis showed that lutein enhanced the Bcl‐2:Bax ratio, inhibited the expression of caspase‐3 and caspase‐9, and increased the protein level of phosphorylated Akt. The network pharmacology and molecular docking prediction results suggested that the phosphoinositide 3‐kinase/protein kinase B (PI3K/Akt) signaling pathway was a potential mechanism of lutein in DE treatment. Furthermore, LY294002, a specific PI3K inhibitor, partially abolished the protective effect of lutein. These results presented that lutein attenuated oxidative damage and apoptosis triggered by MGO in PC12 cells via the PI3K/Akt signaling pathway. Practical applications Lutein is a common carotenoid dispersed in fruits and vegetables. This article confirmed a protective effect of lutein on oxidative damage and apoptosis in PC12 cells after MGO damage. These results indicated that lutein could potentially be developed as a nutraceutical or functional food in the prevention of diabetic‐related neurodegenerative diseases.

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Effect of Diazoxide Preconditioning on Cultured Rat Myocardium Microvascular Endothelial Cells against Apoptosis and Relation of PI3K/Akt Pathway

Cited by 8 publications

References 10 publications

A glucagon-like peptide-1 analog, liraglutide, ameliorates endothelial dysfunction through miRNAs to inhibit apoptosis in rats

A glucagon-like peptide-1 analog, liraglutide, ameliorates endothelial dysfunction through miRNAs to inhibit apoptosis in rats

Can Epigenetics of Endothelial Dysfunction Represent the Key to Precision Medicine in Type 2 Diabetes Mellitus?

Lutein attenuated methylglyoxal‐induced oxidative damage and apoptosis in PC12 cells via the PI3K /Akt signaling pathway

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