Contribution of reactive oxygen species via the OXR1 signaling pathway in the pathogenesis of monocrotaline-induced pulmonary arterial hypertension: The protective role of Crocin

Dianat, Mahin; Radan, Maryam; Mard, Seyyed Ali; Sohrabi, Farzaneh; Saryazdi, Sadaf Sadeghi Nezhad

doi:10.1016/j.lfs.2020.117848

Cited by 17 publications

(16 citation statements)

References 25 publications

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“…Natural herbs and plants also offer many new strategies that target oxidative stress in PAHs. Crocin exerted a protective effect on PAH induced by MCT in rats by regulating the oxidation resistance 1 (OXR1) signaling pathway [74]. Ocimum sanctum (Linn) reduced the expression of thiobarbiturate reactants and Nox1, promoted the release of catalase, and had a beneficial effect on MCT-induced PH in rats [91].…”

Section: Preclinical Strategies: Herbal Treatmentsmentioning

confidence: 99%

Oxidative Stress and Antioxidative Therapy in Pulmonary Arterial Hypertension

Gou

et al. 2022

Molecules

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Pulmonary arterial hypertension (PAH) is clinically characterized by a progressive increase in pulmonary artery pressure, followed by right ventricular hypertrophy and subsequently right heart failure. The underlying mechanism of PAH includes endothelial dysfunction and intimal smooth muscle proliferation. Numerous studies have shown that oxidative stress is critical in the pathophysiology of PAH and involves changes in reactive oxygen species (ROS), reactive nitrogen (RNS), and nitric oxide (NO) signaling pathways. Disrupted ROS and NO signaling pathways cause the proliferation of pulmonary arterial endothelial cells (PAECs) and pulmonary vascular smooth muscle cells (PASMCs), resulting in DNA damage, metabolic abnormalities, and vascular remodeling. Antioxidant treatment has become a main area of research for the treatment of PAH. This review mainly introduces oxidative stress in the pathogenesis of PAH and antioxidative therapies and explains why targeting oxidative stress is a valid strategy for PAH treatment.

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Section: Preclinical Strategies: Herbal Treatmentsmentioning

confidence: 99%

Oxidative Stress and Antioxidative Therapy in Pulmonary Arterial Hypertension

Gou

et al. 2022

Molecules

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“…Downregulated Nrf2, increased lipid peroxidation, and decreased antioxidant capacity were found in the lung tissue of the MCT-induced pH model. Intriguingly, restoration of Nrf2 expression improved the hemodynamic parameters and oxidative stress biomarkers [ 54 ]. Hood et al explored the underlying mechanism of PASMC proliferation induced by serotonin and demonstrated decreased Nrf-2 and catalase activity in PASMCs.…”

Section: Nrf2-mediated Oxidative Stress and Phmentioning

confidence: 99%

Target Nuclear Factor Erythroid 2-Related Factor 2 in Pulmonary Hypertension: Molecular Insight into Application

Qin

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key transcription factor involved in maintaining redox balance and activates the expression of downstream antioxidant enzymes. Nrf2 has received wide attention considering its crucial role in oxidative and electrophilic stress. Large amounts of studies have demonstrated the protective role of Nrf2 activation in various pulmonary hypertension (pH) models. Additionally, various kinds of natural phytochemicals acting as Nrf2 activators prevent the development of pH and provide a novel and promising therapeutic insight for the treatment of pH. In the current review, we give a brief introduction of Nrf2 and focus on the role and mechanism of Nrf2 in the pathophysiology of pH and then review the relevant research of Nrf2 agonists in pH in both experimental research and clinical trials.

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“…Oxidation resistance 1 ( OXR1 ) plays a role in antioxidative stress and has an effect on neurodegenerative diseases ( 29 , 30 ). Increased OXR1 expression can effectively protect against oxidative stress-induced cell damage ( 31 , 32 ).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-668-3p regulates oxidative stress and cell damage induced by Aβ1-42 by targeting the OXR1/p53-p21 axis

Li¹,

Wu²,

Ma³

et al. 2022

Ann Transl Med

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Background Alzheimer’s disease (AD) is the most common type of dementia in old age and has become a serious social and medical problem threatening human health. We aimed to explore the mechanisms underlying AD development by screening for microRNAs (miRNAs) that affect AD progression and examining their role in AD development. Methods Hematoxylin-eosin (HE) staining, immunohistochemistry, and immunofluorescence (IF) were used to analyze the characteristics of the hippocampus, neuron cell separation, and related protein expression in mice. We used Gene Expression Omnibus (GEO) data analysis to screen miRNAs and mRNAs that affect AD progression, and quantitative reverse transcription polymerase chain reaction (RT-qPCR) and western blot analysis to determine changes in miRNA and mRNA levels before and after amyloid β (Aβ)1-42 induction. In addition, we used luciferase analysis to examine miRNA and mRNA binding and the effect of miRNA/mRNA interaction on neuronal cell proliferation. Apoptosis and reactive oxygen species (ROS) levels were examined using Cell Counting Kit-8 analysis and flow cytometry (FCM), respectively. The enzyme-linked immunosorbent assay was used to analyze changes in neuronal cell-secreted oxidative stress-related protein levels through miRNA/mRNA interaction. Results Oxidative stress levels were significantly increased in the AD mouse model. GEO data analysis revealed 67 dysregulated miRNAs, and miR-668-3p was identified as a potential therapeutic target for AD. We found that the AD and Aβ1-42-induced models showed an increase in miR-668-3p and a decrease in oxidation resistance 1 ( OXR1 ) expression. The luciferase analysis results revealed that miR-668-3p may play a role in AD development by targeting OXR1 and promoting intracellular oxidative stress by activating p53-p21 signaling. The final rescue experiment also confirmed that Aβ1-42-induction decreased cell proliferation, increased apoptosis, increased cell cycle arrest, and promoted oxidative stress. Tenovin-1 (TEN) enhanced the effect of Aβ1-42, and the miR-668-3p inhibitor partially alleviated it, although the effect of the miR-668-3p inhibitor was weakened by TEN. Conclusions MiR-668-3p negatively regulated OXR1 expression by targeting OXR1 , affecting p53-p21 protein signaling, and regulating cell damage and oxidative stress induced by Aβ1-42. Therefore, miR-668-3p may be a potential therapeutic target for AD.

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Contribution of reactive oxygen species via the OXR1 signaling pathway in the pathogenesis of monocrotaline-induced pulmonary arterial hypertension: The protective role of Crocin

Cited by 17 publications

References 25 publications

Oxidative Stress and Antioxidative Therapy in Pulmonary Arterial Hypertension

Oxidative Stress and Antioxidative Therapy in Pulmonary Arterial Hypertension

Target Nuclear Factor Erythroid 2-Related Factor 2 in Pulmonary Hypertension: Molecular Insight into Application

MicroRNA-668-3p regulates oxidative stress and cell damage induced by Aβ1-42 by targeting the OXR1/p53-p21 axis

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