scholarly journals Cytoprotective effect of chlorogenic acid against hydrogen peroxide-induced oxidative stress in MC3T3-E1 cells through PI3K/Akt-mediated Nrf2/HO-1 signaling pathway

Oncotarget ◽  
2017 ◽  
Vol 8 (9) ◽  
pp. 14680-14692 ◽  
Author(s):  
Dandan Han ◽  
Wei Chen ◽  
Xiaolong Gu ◽  
Ruixue Shan ◽  
Jiaqi Zou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Chlorogenic Acid ◽  
Signaling Pathway ◽  
Cytoprotective Effect

scholarly journals Cytoprotective Effect of Ligustrum robustum Polyphenol Extract against Hydrogen Peroxide-Induced Oxidative Stress via Nrf2 Signaling Pathway in Caco-2 Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Jiayi Chen ◽  
Fangting He ◽  
Sijing Liu ◽  
Tao Zhou ◽  
Saira Baloch ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Signaling Pathway ◽  
Total Phenolic ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Cytoprotective Effect ◽  
Quinone Oxidoreductase ◽  
Antioxidant Genes ◽  
Nrf2 Signaling Pathway

Ligustrum robustum is a traditional herbal tea that is widely distributed in southwest China. The health effects of L. robustum are characteristics of clearing heat, antioxidant, inducing resurgence, and improving digestion. However, the molecular mechanisms related to these effects, particularly the antioxidant mechanism, have been seldom reported. The objective of this study was to assess antioxidative capacity of L. robustum, and its protective effects and mechanisms against hydrogen peroxide (H2O2) - induced toxicity in Caco-2 cells. Total phenolic contents, free radical scavenging activity, and reducing capacity of L. robustum were measured. The effects of L. robustum on the cell viability and antioxidant defense system were explored. The expression of nuclear factor E2 related factor 2 (Nrf2) and antioxidant genes: quinone oxidoreductase 1 (NQO1), heme oxygenase-1 (HO-1), and glutamate cysteine ligase (GCL) were analyzed by western blot and qPCR. Pretreatment of L. robustum could significantly reduce H2O2-induced toxicity, decrease the level of reactive oxygen species (ROS) and malondialdehyde (MDA), and increase the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GR). By activating the expression of Nrf2 and antioxidant genes (NQO1, HO-1, and GCL), L. robustum exerts cytoprotective effect in Caco-2 cells dealt with H2O2. Therefore, the well-established model of Caco-2 cells demonstrates that L. robustum may modulate the cytoprotective effect against the H2O2-induced oxidative stress through the Nrf2 signaling pathway.

scholarly journals Tea polyphenols ameliorate hydrogen peroxide- and constant darkness-triggered oxidative stress via modulating the Keap1/Nrf2 transcriptional signaling pathway in HepG2 cells and mice liver

RSC Advances ◽  
2017 ◽  
Vol 7 (51) ◽  
pp. 32198-32208 ◽  
Author(s):  
Guoyuan Qi ◽  
Yashi Mi ◽  
Rong Fan ◽  
Runnan Li ◽  
Yiwen Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Signaling Pathway ◽  
Hepg2 Cells ◽  
Tea Polyphenols ◽  
Constant Darkness ◽  
Mice Liver

Tea polyphenols alleviate oxidative stressviamodulating the Keap1/Nrf2 transcriptional signaling pathway in HepG2 cells and the liver of mice kept in constant darkness.

scholarly journals NOX2-Derived Hydrogen Peroxide Impedes the AMPK/Akt-mTOR Signaling Pathway in Parkinson's Disease in Vitro Models

2021 ◽  
Author(s):  
Ruijie Zhang ◽  
Nana Zhang ◽  
Xiaoqing Dong ◽  
Xin Chen ◽  
Jing Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Hydrogen Peroxide ◽  
Parkinson's Disease ◽  
Signaling Pathway ◽  
Neuronal Apoptosis ◽  
Mtor Signaling ◽  
Regulatory Proteins ◽  
Mtor Signaling Pathway ◽  
Compound C

Abstract Oxidative stress is closely related to the pathogenesis of Parkinson's disease (PD), a typical neurodegenerative disease. NADPH oxidase 2 (NOX2) is involved in hydrogen peroxide (H2O2) generation. Recently, we have reported that H2O2 and PD toxins, including 6-hydroxydopamine (6-OHDA), 1-Methyl-4-phenylpyridin-1-ium (MPP+) and rotenone, induce neuronal apoptosis by inhibiting mTOR pathway. Here, we show that 6-OHDA, MPP+ or rotenone induced H2O2 generation by upregulation of NOX2 and its regulatory proteins (p22phox, p40phox, p47phox, p67phox, and Rac1), leading to apoptotic cell death in PC12 cells and primary neurons. Pretreatment with catalase, a H2O2-scavenging enzyme, significantly blocked PD toxins-evoked NOX2-derived H2O2, thereby hindering activation of AMPK, inhibition of Akt/mTOR, induction of apoptosis in neuronal cells. Similar events were also seen in the cells pretreated with Mito-TEMPO, a mitochondria-specific superoxide scavenger, implying a mitochondrial H2O2-dependent mechanism involved. Further research revealed that inhibiting NOX2 with apocynin or silencing NOX2 attenuated the effects of PD toxins on AMPK/Akt/mTOR and apoptosis in the cells. Of importance, ectopic expression of constitutively active Akt or dominant negative AMPKα, or inhibition of AMPK with compound C suppressed PD toxins-induced expression of NOX2 and its regulatory proteins, as well as consequential H2O2 and apoptosis in the cells. Taken together, these results indicate that certain PD toxins can impede the AMPK/Akt-mTOR signaling pathway leading to neuronal apoptosis by eliciting NOX2-derived H2O2. Our findings suggest that neuronal loss in PD may be prevented by regulating of NOX2, AMPK/Akt-mTOR signaling and/or administering antioxidants to ameliorate oxidative stress.

scholarly journals Overexpression of IκBα in cardiomyocytes alleviates hydrogen peroxide-induced apoptosis and autophagy through inhibiting NF-κB activation

2020 ◽  
Author(s):  
Min Han ◽  
Xiao-Cui Chen ◽  
Ming-Hui Sun ◽  
Min-Tao Gai ◽  
Yi-Ning Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Western Blot ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Neonatal Rat ◽  
Cell Counting ◽  
Pyrrolidine Dithiocarbamate ◽  
Induced Apoptosis

Abstract Background: Inflammation and oxidative stress play a predominant role in the initiation and progression of ischemia/reperfusion (I/R) injury, of which nuclear factor kappa B (NF-κB) is a crucial mediator. Overexpression of the inhibitor of κB alpha (IκBα) gene is hypothesized to have protective effects against apoptosis and autophagy in cardiomyocytes subjected to hydrogen peroxide (H2O2) through inhibiting the NF-κB pathway.Methods: The IκBαS32A, S36A gene was transfected via adeno-associated virus serotype 9 (AAV9) delivery into neonatal rat ventricular cardiomyocytes (NRVMs) prior to H2O2 treatment. NRVMs were divided into control, H2O2, GFP +H2O2, IκBα+H2O2, and pyrrolidine dithiocarbamate (PDTC)+H2O2 groups. Nuclear translocation of NF-κB p65 subunit was evaluated by immunofluorescence and Western blot. Cell viability was assessed by Cell Counting Kit-8 assay. Supernatant lactate dehydrogenase (LDH) and intracellular malondialdehyde (MDA) were measured to identify H2O2-stimulated cytotoxicity. Apoptosis was determined by Annexin V-PE/7-AAD staining, and the mitochondrial membrane potential (ΔΨm) was detected by JC-1 staining. Western blot was used to detect apoptosis- and autophagy-related proteins.Results: IκBα transfection significantly increased cell viability and ΔΨm, but decreased the supernatant LDH and cellular MDA levels in cardiomyocytes exposed to H2O2. Meanwhile, IκBα overexpression decreased H2O2-induced apoptosis by upregulating the Bcl-2/Bax ratio and reduced autophagy by downregulating the expression of Beclin-1 and the LC3-Ⅱ/LC3-Ⅰ ratio. These effects partly accounted for the ability of IκBα to inhibit the NF-κB signaling pathway, as evidenced by decreases in p65 phosphorylation and nuclear translocation. Indeed, the effects of inactivation of NF-κB signaling with the specific inhibitor, PDTC, resembled the cardioprotective effects of IκBα during H2O2 stimulation.Conclusion: IκBα overexpression can ameliorate H2O2-induced apoptosis, autophagy, oxidative injury, and ΔΨm loss through inhibition of the NF-κB signaling pathway. These findings suggest that IκBα transfection can successfully resist oxidative stress-induced damage through inhibiting NF-κB activation, which may provide a potential therapeutic target for prevention of myocardial I/R injury.

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