The role of ANXA5 in DBP-induced oxidative stress through ERK/Nrf2 pathway

Zhang, Lei; Qin, Zhiqiang; Li, Ran; Wang, Shangqian; Wang, Wei; Tang, Min; Zhang, Wei

doi:10.1016/j.etap.2019.103236

Cited by 24 publications

(12 citation statements)

References 46 publications

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“…After confirming the effect of butein, we further detected the possible molecular pathways that affected the behavior of butein. Recently, nuclear factor-(erythroid-derived 2-) like 2 (Nrf2) was confirmed to exert cytoprotective role in regulating oxidative stress [41]. The MAPK family, especially ERK was the classical antiapoptotic pathways.…”

Section: Discussionmentioning

confidence: 99%

Butein Inhibits Oxidative Stress Injury in Rats with Chronic Heart Failure via ERK/Nrf2 Signaling

Peng

Pan

2022

Cardiovascular Therapeutics

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Background. Chronic heart failure (CHF) is a serious heart disease resulting from cardiac dysfunction. Oxidative stress is an important factor in aging and disease. Butein, however, has antioxidant properties. To determine the effect of butein on oxidative stress injury in rats, a CHF rat model was established. Methods. The CHF rat model was induced by abdominal aortic coarctation (AAC). Rats in CHF+butein and sham+butein group were given 100 mg/kg butein via gavage every day to detect the effect of butein on oxidative stress injury and myocardial dysfunction. The cardiac structural and functional parameters, including the left ventricular end-systolic dimension (LVESD), the left ventricular end-diastolic dimension (LVEDD), the left ventricular ejection fraction (LVEF), and the left ventricular fractional shortening (LVFS), were measured. Oxidative stress was measured through the production of reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and malondialdehyde (MDA). Cardiac injury markers like creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and aspartate aminotransferase (AST) were evaluated. Hematoxylin and eosin (H&E) staining was used to observe the myocardial cell morphology. The effect of butein on the extracellular signal-regulated kinase (ERK)/nuclear factor-E2 p45-related factor (Nrf2) signaling was confirmed by Western blot analysis. Results. Butein had a significant effect on CHF in animal models. In detail, butein inhibited oxidative stress, relieved cardiac injury, and alleviated myocardial dysfunction. Importantly, butein activated the ERK1/2 pathway, which contributed to Nrf2 activation and subsequent heme oxygenase-1 (HO-1) and glutathione cysteine ligase regulatory subunit (GCLC) induction. Conclusions. In this study, butein inhibits oxidative stress injury in CHF rat model via ERK/Nrf2 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Butein Inhibits Oxidative Stress Injury in Rats with Chronic Heart Failure via ERK/Nrf2 Signaling

Peng

Pan

2022

Cardiovascular Therapeutics

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“…Several studies have reported the role of Nrf2 signaling pathways in the mice models of SCI. The Nrf2/HO‐1/NQO1 signaling axis serves as a robust anti‐oxidant pathway in stress‐activated and age‐related diseases (Zhang et al., 2019 ). Z. Li et al.…”

Section: Discussionmentioning

confidence: 99%

Effect of electroacupuncture on inhibition of inflammatory response and oxidative stress through activating ApoE and Nrf2 in a mouse model of spinal cord injury

et al. 2021

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Introduction: Electroacupuncture protects neurons and myelinated axons after spinal cord injury by mitigating the inflammatory response and oxidative stress, but how it exerts these effects is unclear.Methods and results: Spinal cord injury was induced in C57BL/6 wild-type and apolipoprotein E (ApoE) knockout (ApoE -/-) mice, followed by electroacupuncture or ApoE mimetic peptide COG112 treatment. Mice with spinal cord injury suffered loss of myelinated axons and hindlimb motor function through the detections of Basso mouse scale, histology, and transmission electron microscopy; electroacupuncture partially reversed these effects in wild-type mice but not in ApoE -/mice. Combining exogenous ApoE administration with electroacupuncture significantly mitigated the effects of spinal cord injury in both mouse strains, and these effects were associated with up-regulation of anti-inflammatory cytokines and down-regulation of proinflammatory cytokines which were detected by quantitative reverse transcriptionpolymerase chain reaction. Combination treatment also reduced oxidative stress by up-regulating ApoE and Nrf2/HO-1 signaling pathway through the detections of immunofluorescence and western blot analysis. Conclusions:These results suggest that electroacupuncture protects neurons and myelinated axons following spinal cord injury through an ApoE-dependent mechanism.

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“…In this study, MIF and GDF15 were identified in CM2D and in both MSC CM, respectively. Moreover, proteins found in both CM such as AIFM1, CD9 and GSR have been associated with the maintenance of the redox status [ 48 , 49 , 50 ], whilst ANXA5, CDH13, GDF15 and TIMP2 have shown not only antioxidant but also anti-inflammatory effects [ 35 , 51 , 52 , 53 , 54 ]. Notwithstanding, CM3D consistently showed better results when in combination with Dox compared to the effect of CM2D and Dox.…”

Section: Discussionmentioning

confidence: 99%

The Secretome of Human Neonatal Mesenchymal Stem Cells Modulates Doxorubicin-Induced Cytotoxicity: Impact in Non-Tumor Cells

Serras

Camões

Antunes

et al. 2021

IJMS

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Doxorubicin (Dox) is one of the most widely used treatments for breast cancer, although limited by the well-documented cardiotoxicity and other off-target effects. Mesenchymal stem cell (MSC) secretome has shown immunomodulatory and regenerative properties, further potentiated under 3D conditions. This work aimed to uncover the effect of the MSC-derived secretome from 3D (CM3D) or 2D (CM2D) cultures, in human malignant breast cells (MDA-MB-231), non-tumor breast epithelial cells (MCF10A) and differentiated AC16 cardiomyocytes, co-treated with Dox. A comprehensive proteomic analysis of CM3D/CM2D was also performed to unravel the underlying mechanism. CM3D/CM2D co-incubation with Dox revealed no significant differences in MDA-MB-231 viability when compared to Dox alone, whereas MCF10A and AC16 viability was consistently improved in Dox+CM3D-treated cells. Moreover, neither CM2D nor CM3D affected Dox anti-migratory and anti-invasive effects in MDA-MB-231. Notably, Ge-LC-MS/MS proteomic analysis revealed that CM3D displayed protective features that might be linked to the regulation of cell proliferation (CAPN1, CST1, LAMC2, RANBP3), migration (CCN3, MMP8, PDCD5), invasion (TIMP1/2), oxidative stress (COX6B1, AIFM1, CD9, GSR) and inflammation (CCN3, ANXA5, CDH13, GDF15). Overall, CM3D decreased Dox-induced cytotoxicity in non-tumor cells, without compromising Dox chemotherapeutic profile in malignant cells, suggesting its potential use as a chemotherapy adjuvant to reduce off-target side effects.

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The role of ANXA5 in DBP-induced oxidative stress through ERK/Nrf2 pathway

Cited by 24 publications

References 46 publications

Butein Inhibits Oxidative Stress Injury in Rats with Chronic Heart Failure via ERK/Nrf2 Signaling

Butein Inhibits Oxidative Stress Injury in Rats with Chronic Heart Failure via ERK/Nrf2 Signaling

Effect of electroacupuncture on inhibition of inflammatory response and oxidative stress through activating ApoE and Nrf2 in a mouse model of spinal cord injury

The Secretome of Human Neonatal Mesenchymal Stem Cells Modulates Doxorubicin-Induced Cytotoxicity: Impact in Non-Tumor Cells

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