Aspirin eugenol ester attenuates oxidative injury of vascular endothelial cells by regulating NOS and Nrf2 signalling pathways

Huang, Meizhou; Yang, Yajun; Liu, Xi-Wang; Qin, Zhe; Li, Jianyong

doi:10.1111/bph.14592

Cited by 46 publications

(38 citation statements)

References 45 publications

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“…Similar to the previous results of m, AEE alone did not affect the level of intracellular ATP, while AEE pretreatment significantly inhibited the decrease of intracellular ATP concentration induced by PQ ( Figure 3C). These results suggested that AEE could significantly reduce PQ-induced mitochondrial dysfunction as a threshold effect at 1.0 µM by inhibiting intracellular oxidative stress, which are similar to previous study (Huang et al, 2019).…”

Section: Aee Alleviates Pq-induced Mitochondrial Dysfunction In Brl-3supporting

confidence: 91%

“…All experiments and data analysis were performed according the blinding principles (Altman et al, 1983;Huang et al, 2019). Statistical analyses were performed using SAS 9.2 (SAS Institute Inc., Cary, NC).…”

Section: Discussionmentioning

confidence: 99%

“…et al, 2011;Li J.Y. et al, 2012;Ma et al, 2015;Ma et al, 2017;Huang et al, 2019). The effect of AEE against H 2 O 2 -induced oxidative stress of human umbilical vein endothelial cells (HUVECs) is content with AEEenhanced the expression of Bcl2 and Nrf2 (Huang et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

“…et al, 2012;Ma et al, 2015;Ma et al, 2017;Huang et al, 2019). The effect of AEE against H 2 O 2 -induced oxidative stress of human umbilical vein endothelial cells (HUVECs) is content with AEEenhanced the expression of Bcl2 and Nrf2 (Huang et al, 2019). It has been well documented that AEE could alleviate H 2 O 2induced dysfunction of mitochondria, the generation of ROS production and the increase of apoptosis via enhancing the expression of Bcl2 and Nrf2 (Huang et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

“…The effect of AEE against H 2 O 2 -induced oxidative stress of human umbilical vein endothelial cells (HUVECs) is content with AEEenhanced the expression of Bcl2 and Nrf2 (Huang et al, 2019). It has been well documented that AEE could alleviate H 2 O 2induced dysfunction of mitochondria, the generation of ROS production and the increase of apoptosis via enhancing the expression of Bcl2 and Nrf2 (Huang et al, 2019). It is well known that the dysfunction of mitochondria could release cytochrome C, apoptosis inducing factor (AIF), and other factor into cytoplasm to mediate downstream apoptotic signals causing cell apoptosis (Abate et al, 2019;Hasnat et al, 2019), while the exacerbation of reactive oxygen species (ROS) induced by the dysfunction of mitochondria is also vital incentive of cell apoptosis (Meng et al, 2018;Moradzadeh et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

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Aspirin Eugenol Ester Attenuates Paraquat-Induced Hepatotoxicity by Inhibiting Oxidative Stress

et al. 2020

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Aspirin eugenol ester (AEE) is a new potential drug with anti-inflammatory and antioxidant stress pharmacological activity. Paraquat (PQ) is an effective and commercially important herbicide that is widely used worldwide. However, paraquat is highly toxic and can cause various complications and acute organ damage, such as liver, kidney and lung damage. The purpose of this study was to investigate whether AEE has a protective effect on hepatotoxicity induced by PQ in vivo and in vitro. Cell viability, apoptosis rate, mitochondrial function and intracellular oxidative stress were detected to evaluate the protective effect of AEE on PQ-induced BRL-3A (normal rat hepatocytes) cytotoxicity in vitro. In vivo, AEE pretreatment could attenuate oxidative stress and histopathological changes in rat liver induced by PQ. The results showed that AEE could reduce the hepatotoxicity induced by PQ in vivo and in vitro. AEE reduced PQ-induced hepatotoxicity by inhibiting oxidative stress and maintaining mitochondrial function. This study proved that AEE is an effective antioxidant and can reduce the hepatotoxicity of PQ.

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Section: Aee Alleviates Pq-induced Mitochondrial Dysfunction In Brl-3supporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Aspirin Eugenol Ester Attenuates Paraquat-Induced Hepatotoxicity by Inhibiting Oxidative Stress

et al. 2020

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Modulation of atherosclerosis‐related signaling pathways by Chinese herbal extracts: Recent evidence and perspectives

Liu,

Guo,

Zhang

2024

Phytotherapy Research

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Atherosclerotic cardiovascular disease remains a preeminent cause of morbidity and mortality globally. The onset of atherosclerosis underpins the emergence of ischemic cardiovascular diseases, including coronary heart disease (CHD). Its pathogenesis entails multiple factors such as inflammation, oxidative stress, apoptosis, vascular endothelial damage, foam cell formation, and platelet activation. Furthermore, it triggers the activation of diverse signaling pathways including Phosphatidylinositol 3‐kinase/protein kinase B (PI3K/Akt), NF‐E2‐related factor 2/antioxidant response element (Nrf2/ARE), the Notch signaling pathway, peroxisome proliferator‐activated receptor (PPAR), nucleotide oligo‐structural domain‐like receptor thermoprotein structural domain‐associated protein 3 (NLRP3), silencing information regulator 2‐associated enzyme 1 (Sirt1), nuclear transcription factor‐κB (NF‐κB), Circular RNA (Circ RNA), MicroRNA (mi RNA), Transforming growth factor‐β (TGF‐β), and Janus kinase‐signal transducer and activator of transcription (JAK/STAT). Over recent decades, therapeutic approaches for atherosclerosis have been dominated by the utilization of high‐intensity statins to reduce lipid levels, despite significant adverse effects. Consequently, there is a growing interest in the development of safer and more efficacious drugs and therapeutic modalities. Traditional Chinese medicine (TCM) offers a vital strategy for the prevention and treatment of cardiovascular diseases. Numerous studies have detailed the mechanisms through which TCM active ingredients modulate signaling molecules and influence the atherosclerotic process. This article reviews the signaling pathways implicated in the pathogenesis of atherosclerosis and the advancements in research on TCM extracts for prevention and treatment, drawing on original articles from various databases including Google Scholar, Medline, CNKI, Scopus, and Pubmed. The objective is to furnish a reference for the clinical management of cardiovascular diseases.

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Protective effect of C‐phycocyanin and apo‐phycocyanin subunit on programmed necrosis ofGC‐1 spg cells induced byH₂O₂

Dong

Yang

et al. 2022

Environmental Toxicology

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C-phycocyanin (C-PC) is an effective antioxidant and has an important value in medical research. Oxidative stress is considered to be one of the main underlying mechanisms of cell death, and reducing oxidative stress is one of the strategies to enhance germ cell viability. Herein, we investigated the protective effect and the mechanism of C-PC and apo-phycocyanin subunit on oxidative stress damage induced by H 2 O 2 in GC-1 spg cells. C-PC genes were cloned into the pGEX-4T-1 vectorand transformed into Escherichia coli BL21 to achieve the efficient expression of C-PC subunit.GC-1 spg cells were treated with 600 μM H 2 O 2 for 24 h to establish the oxidative stress damage model. Cell viability was detected by CCK-8. The degree of oxidative stress was detected by testing Superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and glutathione (GSH) and Malondialdehyde (MDA) levels. Reactive oxygen species (ROS) was evaluated utilizingby 2', 7'-dichlorofluorescentdiacetate (DCFH-DA). Mitochondrial membrane potential was determined by JC-1.Cell necrosis rate was detected by Annexin V-FITC/PI. Expression of protein was detected by western blot. We found that C-PC and GST-CPC β significantly inhibited H 2 O 2 -induced oxidative damage of GC-1 spg cells, improved the ability of antioxidation, reduced ROS overproduction, and mitochondrial membrane potential loss, and inhibited the RIP-1/RIP-3/ p-MLKL signaling pathway to reduce the necrosis rate. The results demonstrated that C-PC played a protective role against H 2 O 2induced cell damage, especially its β subunit. This study provides a theoretical basis for C-PC as a potential protective agent of reproductive system.

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Aspirin eugenol ester attenuates oxidative injury of vascular endothelial cells by regulating NOS and Nrf2 signalling pathways

Cited by 46 publications

References 45 publications

Aspirin Eugenol Ester Attenuates Paraquat-Induced Hepatotoxicity by Inhibiting Oxidative Stress

Aspirin Eugenol Ester Attenuates Paraquat-Induced Hepatotoxicity by Inhibiting Oxidative Stress

Modulation of atherosclerosis‐related signaling pathways by Chinese herbal extracts: Recent evidence and perspectives

Protective effect of C‐phycocyanin and apo‐phycocyanin subunit on programmed necrosis ofGC‐1 spg cells induced byH₂O₂

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Aspirin eugenol ester attenuates oxidative injury of vascular endothelial cells by regulating NOS and Nrf2 signalling pathways

Cited by 46 publications

References 45 publications

Aspirin Eugenol Ester Attenuates Paraquat-Induced Hepatotoxicity by Inhibiting Oxidative Stress

Aspirin Eugenol Ester Attenuates Paraquat-Induced Hepatotoxicity by Inhibiting Oxidative Stress

Modulation of atherosclerosis‐related signaling pathways by Chinese herbal extracts: Recent evidence and perspectives

Protective effect of C‐phycocyanin and apo‐phycocyanin subunit on programmed necrosis ofGC‐1 spg cells induced byH2O2

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Product

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Protective effect of C‐phycocyanin and apo‐phycocyanin subunit on programmed necrosis ofGC‐1 spg cells induced byH₂O₂