scholarly journals Assessing the Potential Value and Mechanism of Kaji-Ichigoside F1 on Arsenite-Induced Skin Cell Senescence

2022 ◽  
Vol 2022 ◽  
pp. 1-16
Author(s):  
Qibing Zeng ◽  
Sufei Du ◽  
Yuyan Xu ◽  
Fan Yang ◽  
Liping Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Antioxidant Enzyme ◽  
Signaling Pathway ◽  
Exposed Group ◽  
Cell Senescence ◽  
Lipid Peroxidation Product ◽  
Effective Prevention ◽  
Arsenic Poisoning ◽  
Skin Cell

Chronic exposure to inorganic arsenic is a major environmental public health issue worldwide affecting more than 220 million of people. Previous studies have shown the correlation between arsenic poisoning and cellular senescence; however, knowledge regarding the mechanism and effective prevention measures has not been fully studied. First, the associations among the ERK/CEBPB signaling pathway, oxidative stress, and arsenic-induced skin cell senescence were confirmed using the HaCaT cell model. In the arsenic-exposed group, the relative mRNA and protein expressions of ERK/CEBPB signaling pathway indicators (ERK1, ERK2, and CEBPB), cell cycle-related genes (p21, p16INK4a), and the secretion of SASP (IL-1α, IL-6, IL-8, TGF-β1, MMP-1, MMP-3, EGF, and VEGF) and the lipid peroxidation product (MDA) were significantly increased in cells ( P < 0.05 ), while the activity of antioxidant enzyme (SOD, GSH-Px, and CAT) was significantly decreased ( P < 0.05 ), and an increased number of cells accumulated in the G1 phase ( P < 0.05 ). Further Kaji-ichigoside F1 intervention experiments showed that compared to that in the arsenic-exposed group, the expression level of the activity of antioxidant enzyme was significantly increased in the Kaji-ichigoside F1 intervention group ( P < 0.05 ), but the indicators of ERK/CEBPB signaling pathway, cell cycle-related genes, and SASP were significantly decreased ( P < 0.05 ), and the cell cycle arrest relieved to a certain extent ( P < 0.05 ). Our study provides some limited evidence that the ERK/CEBPB signaling pathway is involved in low-dose arsenic-induced skin cell senescence, through regulating oxidative stress. The second major finding was that Kaji-ichigoside F1 can downregulate the ERK/CEBPB signaling pathway and regulate the balance between oxidation and antioxidation, alleviating arsenic-induced skin cell senescence. This study provides experimental evidence for further understanding of Kaji-ichigoside F1, a natural medicinal plant that may be more effective in preventing and controlling arsenic poisoning.

scholarly journals Transcriptomic Analysis Reveals Both Coxsackievirus B3 Woodruff and GD Strain Using Similar Key Genes to Induce FoxO Signaling Pathway Activation in HeLa Cells

2021 ◽  
Author(s):  
Mi Liu ◽  
Qian Yang ◽  
Jun Han
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Signaling Pathway ◽  
Hela Cells ◽  
Stress Resistance ◽  
Coxsackievirus B3 ◽  
Common Mechanism ◽  
Oxidative Stress Resistance ◽  
Key Genes ◽  
Foxo Signaling Pathway

Abstract Coxsackievirus B3 (CVB3) is the major cause of viral myocarditis in human worldwide. Various studies have investigated the viral infection and pathogenic mechanisms. However, the precise disease mechanism is still not clear. In this study, RNA-seq technology was used to compare the transcriptomic profile of virus infected HeLa cells to the controls in order to analysis the key genes of host virus interaction. Two CVB3 strains, CVB3 Woodruff and GD16-69-CVB3 strain were selected to figure out the common disease mechanisms of both experimental and clinical strains respectively. Increased expression of cell cycle genes CCNG2, GADD45B, PIM1, RBM15, KLF10 and RIOK3, down regulation of CYBA were detected. Autophagy genes ATG12 and YOD1 were also upregulated during CVB3 infection. Slightly increase of SOD2 and ATG12 were shown in the expression of infected cells, meanwhile, little change was detected in GABARAP expression. Further, FoxO signaling pathway was enriched by KEGG analysis, shown a close interaction with the DEGs in the PPI network. Genes of related pathways such as cell cycle, autophagy and oxidative stress resistance were confirmed by RT-PCR as well. In conclusion, our results reveal that FoxO signaling pathway is a common mechanism activated during the infection of both CVB3 strains. And this pathway plays a regulatory role in downstream pathways such as cell cycle, autophagy, oxidative stress resistance and antiviral immune responds.

scholarly journals Identification of aSaccharomyces cerevisiaeGene that Is Required for G1 Arrest in Response to the Lipid Oxidation Product Linoleic Acid Hydroperoxide*

2001 ◽  
Vol 12 (6) ◽  
pp. 1801-1810 ◽  
Author(s):  
Nazif Alic ◽  
Vincent J. Higgins ◽  
Ian W. Dawes
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Linoleic Acid ◽  
Cell Cycle Arrest ◽  
Stress Responses ◽  
G1 Arrest ◽  
Linoleic Acid Hydroperoxide ◽  
Lipid Peroxidation Product ◽  
Cycle Arrest ◽  
Acid Hydroperoxide

Reactive oxygen species cause damage to all of the major cellular constituents, including peroxidation of lipids. Previous studies have revealed that oxidative stress, including exposure to oxidation products, affects the progression of cells through the cell division cycle. This study examined the effect of linoleic acid hydroperoxide, a lipid peroxidation product, on the yeast cell cycle. Treatment with this peroxide led to accumulation of unbudded cells in asynchronous populations, together with a budding and replication delay in synchronous ones. This observed modulation of G1 progression could be distinguished from the lethal effects of the treatment and may have been due to a checkpoint mechanism, analogous to that known to be involved in effecting cell cycle arrest in response to DNA damage. By examining several mutants sensitive to linoleic acid hydroperoxide, theYNL099c open reading frame was found to be required for the arrest. This gene (designated OCA1) encodes a putative protein tyrosine phosphatase of previously unknown function. Cells lacking OCA1 did not accumulate in G1 on treatment with linoleic acid hydroperoxide, nor did they show a budding, replication, or Start delay in synchronous cultures. Although not essential for adaptation or immediate cellular survival,OCA1 was required for growth in the presence of linoleic acid hydroperoxide, thus indicating that it may function in linking growth, stress responses, and the cell cycle. Identification ofOCA1 establishes cell cycle arrest as an actively regulated response to oxidative stress and will enable further elucidation of oxidative stress-responsive signaling pathways in yeast.

scholarly journals Deoxynivalenol induces apoptosis and autophagy in human prostate epithelial cells via PI3K/Akt signaling pathway

2021 ◽  
Author(s):  
Karolina Kowalska ◽  
Marta Justyna Kozieł ◽  
Dominika Ewa Habrowska-Górczyńska ◽  
Kinga Anna Urbanek ◽  
Kamila Domińska ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Dna Damage ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Cycle Phase ◽  
Akt Signaling Pathway ◽  
Normal Prostate ◽  
Prostate Epithelial Cells

AbstractPhosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway is one of the most deregulated signaling pathway in prostate cancer. It controls basic processes in cells: cell proliferation and death. Any disturbances in the balance between cell death and survival might result in carcinogenesis. Deoxynivalenol (DON) is one of the most common mycotoxins, a toxic metabolites of fungi, present in our everyday diet and feed. Although previous studies reported DON to induce oxidative stress, modulate steroidogenesis, DNA damage and cell cycle modulation triggering together its toxicity, its effect on normal prostate epithelial cells is not known. The aim of the study was to evaluate the effect of DON on the apoptosis and autophagy in normal prostate epithelial cells via modulation of PI3K/Akt signaling pathway. The results showed that DON in a dose of 30 µM and 10 µM induces oxidative stress, DNA damage and cell cycle arrest in G2/M cell cycle phase. The higher concentration of DON induces apoptosis, whereas lower one autophagy in PNT1A cells, indicating that modulation of PI3K/Akt by DON results in the induction of autophagy triggering apoptosis in normal prostate epithelial cells.

scholarly journals Chronic oxidative stress sensitizes hepatocytes to death from 4-hydroxynonenal by JNK/c-Jun overactivation

2009 ◽  
Vol 297 (5) ◽  
pp. G907-G917 ◽  
Author(s):  
Rajat Singh ◽  
Yongjun Wang ◽  
Jörn M. Schattenberg ◽  
Youqing Xiang ◽  
Mark J. Czaja
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Fatty Liver ◽  
Signaling Pathway ◽  
Oxidant Stress ◽  
Mitogen Activated Protein Kinase ◽  
Synthetase Activity ◽  
Lipid Peroxidation Product ◽  
Jnk Signaling ◽  
Peroxidation Product

Sustained activation of the c-Jun NH2-terminal kinase (JNK) signaling pathway mediates the development and progression of experimental diet-induced nonalcoholic fatty liver disease (NAFLD). Delineating the mechanism of JNK overactivation in the setting of a fatty liver is therefore essential to understanding the pathophysiology of NAFLD. Both human and experimental NAFLD are associated with oxidative stress and resultant lipid peroxidation, which have been proposed to mediate the progression of this disease from simple steatosis to steatohepatitis. The ability of oxidants and the lipid peroxidation product 4-hydroxynonenal (HNE) to activate JNK signaling suggested that these two factors may act synergistically to trigger JNK overactivation. The effect of HNE on hepatocyte injury and JNK activation was therefore examined in cells under chronic oxidant stress from overexpression of the prooxidant enzyme cytochrome P450 2E1 (CYP2E1), which occurs in NAFLD. CYP2E1-generated oxidant stress sensitized a rat hepatocyte cell line to death from normally nontoxic concentrations of HNE. CYP2E1-overexpressing cells underwent a more profound depletion of glutathione (GSH) in response to HNE secondary to decreased γ-glutamylcysteine synthetase activity. GSH depletion led to overactivation of JNK/c-Jun signaling at the level of mitogen-activated protein kinase kinase 4 that induced cell death. Oxidant stress and the lipid peroxidation product HNE cause synergistic overactivation of the JNK/c-Jun signaling pathway in hepatocytes, demonstrating that HNE may not be just a passive biomarker of hepatic oxidant stress but rather an active mediator of hepatocellular injury through effects on JNK signaling.

scholarly journals Lentiviral Vector-Mediated SHC3 Silencing Exacerbates Oxidative Stress Injury in Nigral Dopamine Neurons by Regulating the PI3K-AKT-FoxO Signaling Pathway in Rats with Parkinson’s Disease

2018 ◽  
Vol 49 (3) ◽  
pp. 971-984 ◽  
Author(s):  
Jian Gong ◽  
Lei Zhang ◽  
Qian Zhang ◽  
Xiang Li ◽  
Xiang-Jun Xia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Cell Cycle Progression ◽  
Dopamine Neurons ◽  
Cycle Progression ◽  
Foxo Signaling Pathway

Background/Aims: Parkinson’s disease (PD) is a prevalent disease that leads to motor and cognitive disabilities, and oxidative stress (OS) injury was found to be related to the etiology of PD. Increasing evidence has shown that SHC3 is aberrantly expressed in neurons. The current study examines the involvement of SHC3 silencing in OS injury in the nigral dopamine neurons in rats with PD via the PI3K-AKT-FoxO signaling pathway. Methods: To study the mechanisms and functions of SHC3 silencing in PD at the tissue level, 170 rats were selected, and a lentivirus-based packaging system was designed to silence SHC3 expression in rats. Furthermore, PC12 cells were selected for in vitro experimentation. To evaluate the effect of SHC3 silencing in nigral dopamine neuronal growth, an MTT assay, propidium iodide (PI) single staining and Annexin V-PI double staining were performed to detect cell viability, cell cycle progression and cell apoptosis, respectively. Results: SHC3 shRNA led to decreased SOD and MDA levels and enhanced GSH activity, indicating that SHC3 silencing leads to motor retardation. SHC3 silencing repressed the extent of Akt and FoxO phosphorylation, thereby inhibiting the PI3K-AKT-FoxO signaling pathway. Furthermore, in cell experiments, SHC3 silencing suppressed PC12 cell proliferation and cell cycle progression, whereas it enhanced cell apoptosis. Conclusion: The current study provides evidence suggesting that SHC3 silencing may aggravate OS injury in nigral dopamine neurons via downregulation of the PI3K-AKT-FoxO signaling pathway in PD rats.

The Dinitrophenol and Potassium Iodate Influence on Hordeum Vulgare Seedlings Viability\

2018 ◽  
Vol 69 (8) ◽  
pp. 2160-2166
Author(s):  
Elena Todirascu Ciornea ◽  
Gabriela Dumitru ◽  
Ion Sandu
Keyword(s):  
Oxidative Stress ◽  
Hordeum Vulgare ◽  
Antioxidant Enzyme ◽  
Oxygen Radicals ◽  
Free Oxygen Radicals ◽  
Potassium Iodate ◽  
Free Oxygen ◽  
Oxidative Stress Enzymes ◽  
Stress Enzymes ◽  
Seeds Germination

The using of the pesticides of dinitrophenol type in agriculture has as consequence the major pollution of the environment, the plants taking these substances from the soil and once with these ones they reach in the human and animal organism where they product disequilibrium that are interpreted through the accumulation of free oxygen radicals with direct repercussions on the antioxidant enzyme�s synthesis intensification and on their activity�s increase. The apply of treatments on the barley seeds had significant effects regarding the seeds� germination, the young plants� growth, the oxidative stress enzymes� activity, but also regarding the content of photoassimilators and carotenoids pigments.

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