Dehydroepiandrosterone rehabilitate BRL‐3A cells oxidative stress damage induced by hydrogen peroxide

Li, Longlong; Zhao, Jinlong; Ge, Chongyang; Yu, Lei; Ma, Haitian

doi:10.1002/jcp.26458

Cited by 13 publications

(7 citation statements)

References 42 publications

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“…Taken together, these results showed that phlorizin decreased the cell apoptosis by downregulating the expression of Caspase 3 and Caspase 9 genes and upregulating the expression of Bcl‐2 gene. This phenomenon was similar to that in a previous study ( Li, Zhao, et al, ), which stated that dehydroepiandrosterone relieves oxidative damage by decreasing the expression of apoptosis genes and increasing the expression of anti‐apoptosis gene in H 2 O 2 ‐induced BRL‐3A cells.…”

Section: Discussionsupporting

confidence: 91%

Protective effect of apple phlorizin on hydrogen peroxide‐induced cell damage in HepG2 cells

et al. 2019

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Apple phlorizin has many biological activities, such as antioxidant and liver protection. The present study aimed to evaluate the roles of apple phlorizin against hydrogen peroxide (H2O2)‐induced oxidative damage in HepG2 cells. In this study, treatment with apple phlorizin (100 and 150 μg/ml) decreased the production of reactive oxygen species and alleviated apoptosis as well as DNA damage in H2O2‐induced HepG2 cells. These effects were associated with the increased activity of antioxidant enzymes, enhanced the ARE‐driven phase II antioxidant gene expression and its upstream Nrf2 protein expression, and decreased apoptosis‐related gene expression. However, the phase II antioxidant gene expression and Nrf2 protein expression upregulated by phlorizin were reversed by Nrf2 shRNA transfection. These results showed that phlorizin relieves oxidative stress, DNA damage, and apoptosis in H2O2‐induced HepG2 cells, at least partially, by regulating the expression of Nrf2 protein and apoptosis‐related genes. Practical applications Apple phlorizin is a polyphenol compound extracted from apple or apple juice. This report highlighted a protective effect of phlorizin on antioxidant stress, DNA damage, and apoptosis in H2O2‐induced HepG2 cells. These results suggested that phlorizin may be developed for functional foods.

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Section: Discussionsupporting

confidence: 91%

Protective effect of apple phlorizin on hydrogen peroxide‐induced cell damage in HepG2 cells

et al. 2019

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“…In order to simulate oxidative injury in vascular endothelial cells in vivo, many oxidative stress models of endothelial cells have been established. H 2 O 2 ‐induced oxidative stress is well established as a common model for oxidative injury (Kaczara et al, ; Li, Zhao, Ge, Yu, & Ma, ). In the present study, apoptosis of HUVECs showed a dose‐dependent relationship with H 2 O 2 .…”

Section: Discussionmentioning

confidence: 99%

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

Huang

Yang

Liu

et al. 2019

British J Pharmacology

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Background and Purpose: Aspirin eugenol ester (AEE) is a new drug compound synthesized by combining aspirin with eugenol. It was reported to possess antithrombotic, anti-atherosclerotic, and anti-oxidative effects. However, its molecular mechanism against oxidative injury is unclear. This study investigated how AEE affected the oxidative injury of vascular endothelial cells in vivo and in vitro. Experimental Approach: A hamster model of atherosclerosis induced by a high fat diet (HFD) and an in vitro model of oxidative stress, H 2 O 2 -induced apoptosis of HUVECs, were used to investigate the anti-oxidative effects of AEE. Key Results: AEE significantly reduced the stimulatory effect of HFD on malondialdehyde, the inhibitory effect of HFD on SOD activity and GSH/GSSG ratio, and the overexpression of inducible NOS (iNOS) in the aorta. In vitro, incubation of HUVECs with H 2 O 2 led their apoptosis, dysfunctions of the NO systems (including increased iNOS activity, decreased endothelial NOS activity, and increased production of NO), an imbalance in calcium homeostasis and energy metabolism with an increase in intracellular free calcium and decrease in ATP, and a down-regulation of Nrf2. In contrast, in the HUVECs pretreated with 1 μM AEE for 24 hr, the above adverse effects induced by H 2 O 2 were significantly ameliorated. Moreover, the decrease in NO production and activity of iNOS induced by AEE was significantly attenuated in Nrf2-inhibited HUVECs.Conclusion and Implication: AEE protects vascular endothelial cells from oxidative injury by regulating NOS and Nrf2 signalling pathways. This suggests that AEE is a novel potential agent for the prevention of atherosclerosis.

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“…BRL-3A cells were pretreated with vehicle, 10 μ M Trilostane, 10 μ M Flutamide, or 1 μ M Fulvestrant for 60 min. The cells were then treated with DHEA (0, 1, 10, or 100 μ M), testosterone (12.0 nM), or estradiol (6.3 nM) for 24 h and subsequently treated with 150 μ M H 2 O 2 for another 2 h. Intracellular ROS content was analyzed with the fluoroprobe 2′,7′-dichlorodihydrofluorescein diacetate (H2DCF-DA) and dihydroethidium (DHE) as shown in our recent reports [16, 17]. Briefly, BRL-3A cells were incubated with H2DCF-DA for 30 min at 37°C, washed three times, and resuspended in cold PBS, after which they were immediately subjected to flow cytometry analysis with FACSCalibur™ (Becton Dickinson, San Jose, USA).…”

Section: Methodsmentioning

confidence: 99%

“…The cell treatments were the same as described in Section 2.4 for ROS analysis, and cell apoptosis was examined as reported in our studies [16, 17]. Briefly, BRL-3A cells were collected and washed with cold PBS, placed in 195 μ L Annexin V-FITC binding solution, incubated in 5 μ L Annexin V-FITC and 10 μ L propidium iodide in the dark for 30 min, and immediately subjected to flow cytometry analysis with FACSCalibur™.…”

Section: Methodsmentioning

confidence: 99%

“…In fact, the decrease in circulating DHEA levels is associated with multiple metabolic consequences including autoimmune diseases, aberrations in lipid metabolism, type 2 diabetes, and oxidative stress-related diseases [9]. Recently, DHEA was reported to exhibit antioxidative effects under conditions of acute as well as chronic oxidative stress [10–12], and these antioxidant effects have been confirmed through in vivo [13, 14] and in vitro [15] experiments, including our recent study in which DHEA treatment was found to protect various types of cells against oxidative damage [16, 17]. Although these beneficial effects of DHEA are known, there is not enough information about the mechanisms through which it exerts these effects.…”

Section: Introductionmentioning

confidence: 94%

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Dehydroepiandrosterone Prevents H₂O₂-Induced BRL-3A Cell Oxidative Damage through Activation of PI3K/Akt Pathways rather than MAPK Pathways

Yao

Jiang

et al. 2019

Oxidative Medicine and Cellular Longevity

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Dehydroepiandrosterone (DHEA) is a popular dietary supplement that has well-known benefits in animals and humans, but there is not enough information about the mechanisms underlying its effects. The present study aimed at investigating these mechanisms through in vitro experiments on the effects of DHEA on rat liver BRL-3A cells exposed to oxidative stress through H2O2. The findings showed that DHEA increased the antioxidant enzyme activity, decreased ROS generation, and inhibited apoptosis in H2O2-treated cells. These effects of DHEA were not observed when the cells were pretreated with known antagonists of sex hormones (Trilostane, Flutamide, or Fulvestrant). Furthermore, treatment with estradiol and testosterone did not have the same protective effects as DHEA. Thus, the beneficial effects of DHEA were associated with mechanisms that were independent of steroid hormone pathways. With regard to the mechanism underlying the antiapoptotic effect of DHEA, pretreatment with DHEA was found to induce a significant decrease in the protein expression of Bax and caspase-3 and a significant increase in the protein expression of PI3K and p-Akt in H2O2-treated BRL-3A cells. These effects of DHEA were abolished when the cells were pretreated with the PI3K inhibitor LY294002. No changes were observed on the p-ERK1/2, p-p38, and p-JNK protein levels in H2O2-induced BRL-3A cells pretreated with DHEA. In conclusion, our data demonstrate that DHEA protects BRL-3A cells against H2O2-induced oxidative stress and apoptosis through mechanisms that do not involve its biotransformation into steroid hormones or the activation of sex hormone receptors. Importantly, the protective effect of DHEA on BRL-3A cells was mainly associated with PI3K/Akt signaling pathways, rather than MAPK signaling pathways.

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Dehydroepiandrosterone rehabilitate BRL‐3A cells oxidative stress damage induced by hydrogen peroxide

Cited by 13 publications

References 42 publications

Protective effect of apple phlorizin on hydrogen peroxide‐induced cell damage in HepG2 cells

Protective effect of apple phlorizin on hydrogen peroxide‐induced cell damage in HepG2 cells

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

Dehydroepiandrosterone Prevents H₂O₂-Induced BRL-3A Cell Oxidative Damage through Activation of PI3K/Akt Pathways rather than MAPK Pathways

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Dehydroepiandrosterone rehabilitate BRL‐3A cells oxidative stress damage induced by hydrogen peroxide

Cited by 13 publications

References 42 publications

Protective effect of apple phlorizin on hydrogen peroxide‐induced cell damage in HepG2 cells

Protective effect of apple phlorizin on hydrogen peroxide‐induced cell damage in HepG2 cells

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

Dehydroepiandrosterone Prevents H2O2-Induced BRL-3A Cell Oxidative Damage through Activation of PI3K/Akt Pathways rather than MAPK Pathways

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Dehydroepiandrosterone Prevents H₂O₂-Induced BRL-3A Cell Oxidative Damage through Activation of PI3K/Akt Pathways rather than MAPK Pathways