The effects of flavonoids on human first trimester trophoblast spheroidal stem cell self-renewal, invasion and JNK/p38 MAPK activation: Understanding the cytoprotective effects of these phytonutrients against oxidative stress

Ebegboni, Vernon Justice; Balahmar, Reham M.; Dickenson, John M.; Sivasubramaniam, Shiva

doi:10.1016/j.bcp.2019.04.023

Cited by 25 publications

(20 citation statements)

References 71 publications

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“…The p38MAPK signaling pathway has been reported to be related to the growth and migration of trophoblasts. For example, a study by Zhou et al [20] has revealed that transforming growth factor-β1 could inhibit the apoptosis of trophoblasts induced by mercuric chlorides by suppressing the p38MAPK signaling pathway, and one other study by Ebegboni et al [21] also reported that flavonoids promoted the self-renewal and invasion of spherical stem cells of trophoblasts by inhibiting p38MAPK 5 Computational and Mathematical Methods in Medicine signaling pathway. In addition, one study by Che et al [22] also found that knockout of heparanase gene inhibits the invasion of human trophoblasts by activating the p38MAPK signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Efficacy of Low Molecular Heparin on Preeclampsia by Inhibiting Apoptosis of Trophoblasts via the p38MAPK Signaling Pathway

Quan

Zuo

2021

Computational and Mathematical Methods in Medicine

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Objective. To explore the efficacy of low molecular heparin on preeclampsia by inhibiting apoptosis of trophoblasts via the p38MAPK signaling pathway. Methods. A preeclampsia rat model was established, and the effects of low molecular heparin on preeclampsia via the p38MAPK signaling pathway were analyzed based on intervention of the rats with different combinations of low molecular heparin and p38MAPK signaling pathway activator. Furthermore, a hypoxia/reoxygenation model of trophoblasts in vitro was established to explore the effects of low molecular heparin on trophoblasts via the p38MAPK signaling pathway. Results. After treatment with low molecular heparin, pregnant rats in the heparin group showed significantly decreased blood pressure, 24 h proteinuria, and p38MAPK protein levels in placenta tissues and decreased apoptosis rate of placenta tissue cells (all P < 0.05 ) and showed more fetal rats and lowered weight of them (both P < 0.05 ) but showed no significant change in the weight of placenta (all P > 0.05 ). Pregnant rats treated with low molecular heparin and p38MAPK activator showed significantly higher blood pressure, 24 h proteinuria, and p38MAPK protein levels in placenta tissues and apoptosis rate of placenta tissue cells than those of pregnant rats in the heparin group (all P < 0.05 ) and also showed less fetal rats and lighter fetal rats than those in the heparin group (both P < 0.05 ) but showed no difference with them in the weight of placenta ( P > 0.05 ). Further analysis revealed that low molecular heparin could protect the survival and migration of trophoblasts under hypoxia/reoxygenation conditions and reduce apoptosis of them (all P < 0.05 ). Conclusion. Low molecular heparin can alleviate preeclampsia by inhibiting the p38MAPK signaling pathway and can inhibit apoptosis of trophoblasts and promote proliferation and migration of them.

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Section: Discussionmentioning

confidence: 99%

Efficacy of Low Molecular Heparin on Preeclampsia by Inhibiting Apoptosis of Trophoblasts via the p38MAPK Signaling Pathway

Quan

Zuo

2021

Computational and Mathematical Methods in Medicine

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“…Additionally, flavonoids can control the redox imbalance by regulating the antioxidant enzyme gene expression via Nrf2/ARE (nuclear erythroid 2-related factor 2/antioxidant response element) signaling pathway [ 144 , 145 ], and the activity of multiple cellular signaling pathways, such as Extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) [ 42 , 146 , 147 ], c-Jun N-terminal kinases (JNK) [ 146 , 148 ], phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) [ 42 , 138 , 149 ], and mitogen-activated protein kinase (p38 MAPK) signaling pathway [ 148 , 150 ]. Moreover, flavonoids can suppress apoptosis and excessive inflammatory responses, thereby reducing the ROS that is incidentally generated by the activation of a cytotoxic mechanism ( Figure 2 ) [ 43 , 138 , 151 , 152 , 153 , 154 , 155 ].…”

Section: Natural Antioxidants: Flavonoidsmentioning

confidence: 99%

Control of Reactive Oxygen Species for the Prevention of Parkinson’s Disease: The Possible Application of Flavonoids

et al. 2020

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Oxidative stress reflects an imbalance between the production of reactive oxygen species (ROS) and antioxidant defense systems, and it can be associated with the pathogenesis and progression of neurodegenerative diseases such as multiple sclerosis, stroke, and Parkinson’s disease (PD). The application of antioxidants, which can defend against oxidative stress, is able to detoxify the reactive intermediates and prevent neurodegeneration resulting from excessive ROS production. There are many reports showing that numerous flavonoids, a large group of natural phenolic compounds, can act as antioxidants and the application of flavonoids has beneficial effects in the adult brain. For instance, it is well known that the long-term consumption of the green tea-derived flavonoids catechin and epigallocatechin gallate (EGCG) can attenuate the onset of PD. Also, flavonoids such as ampelopsin and pinocembrin can inhibit mitochondrial dysfunction and neuronal death through the regulation of gene expression of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Additionally, it is well established that many flavonoids exhibit anti-apoptosis and anti-inflammatory effects through cellular signaling pathways, such as those involving (ERK), glycogen synthase kinase-3β (GSK-3β), and (Akt), resulting in neuroprotection. In this review article, we have described the oxidative stress involved in PD and explained the therapeutic potential of flavonoids to protect the nigrostriatal DA system, which may be useful to prevent PD.

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“…Apoptosis is programmed cell death and plays an important role in maintaining cell homeostasis (Ebegboni et al 2019). Apoptosis is also regulated by many genes, the Bcl-2 is a potent inhibitor of apoptosis and plays a regulatory role in the process of cell apoptosis (Krishnaswamy Kannan 2000).…”

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confidence: 99%

The toxicity of cooking oil fumes on human bronchial epithelial cells through ROS‐mediated MAPK, NF‐κB signaling pathways and NLRP3 inflammasome

Liu

Miao

et al. 2022

Environmental Toxicology

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Cooking oil fumes (COFs) are main pollutants in kitchen and indoor air, which threaten human health.Exposure to COFs can cause respiratory diseases and impair pulmonary function. To investigate the toxicity of COFs on human bronchial epithelial cells (Beas-2B) and explore the underlying mechanisms, MTT assay was conducted to detect the viability of Beas-2B. Intracellular reactive oxygen species (ROS) levels and nitric oxide (NO) levels were determined with DCFH-DA assay and DAF-FM assay. The expression of genes involved in in ammation were measured with quantitative real-time PCR (qRT-PCR).The phosphorylation and the expression of proteins related to Mitogen-activated protein kinase (MAPK), NF-κB signaling pathways were measured with western blot. Our results revealed that COFs decreased Beas-2B cells viability, increased the ROS levels and NO levels in cells and induced apoptosis in Beas-2B cells. The results of qRT-PCR and western blot showed that the expression of NLRP3, p65, iNOS, IL-1β, and the factors related to oxidative stress and in ammation increased, NF-κB signaling pathway and MAPK signaling pathway were activated. This study provided some useful information to alleviate the toxicity of COFs and revealed the possible mechanism for the damage on respiratory system induced by COFs. et al. 2015;Wang et al. 2018).COFs pollution produced by cooking usually includes ketones, aldehydes, hydrocarbons, fatty acids, alcohols, aromatic compounds, esters, heterocycles, and lactones is a serious health risk in china due to the cooking manners (Ding et al. 2020;Lee and Gany 2013). In China alone, the number of people exposed to COFs in 2018 has reached to 240 million and most of whom were middle-aged women . Women exposed to COFs are at higher risk for chronic bronchitis, for pregnant women, such exposure can also affect the fetus and increase the risks of adverse birth outcomes (Hou et al. 2018;Vavalà et al. 2014;Zhu et al. 2019). Studies have shown that exposure to COFs increased the risk of respiratory diseases, such as airway infection, chronic obstructive pulmonary disease, tuberculosis and

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The effects of flavonoids on human first trimester trophoblast spheroidal stem cell self-renewal, invasion and JNK/p38 MAPK activation: Understanding the cytoprotective effects of these phytonutrients against oxidative stress

Cited by 25 publications

References 71 publications

Efficacy of Low Molecular Heparin on Preeclampsia by Inhibiting Apoptosis of Trophoblasts via the p38MAPK Signaling Pathway

Efficacy of Low Molecular Heparin on Preeclampsia by Inhibiting Apoptosis of Trophoblasts via the p38MAPK Signaling Pathway

Control of Reactive Oxygen Species for the Prevention of Parkinson’s Disease: The Possible Application of Flavonoids

The toxicity of cooking oil fumes on human bronchial epithelial cells through ROS‐mediated MAPK, NF‐κB signaling pathways and NLRP3 inflammasome

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