scholarly journals Decorin inhibits glucose-induced lens epithelial cell apoptosis via suppressing p22phox-p38 MAPK signaling pathway

2019 ◽  
Author(s):  
Shanshan Du ◽  
Jingzhi Shao ◽  
Dandan Xie ◽  
Fengyan Zhang
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
P38 Mapk ◽  
Stress Level ◽  
High Glucose ◽  
Lens Epithelial Cell ◽  
Human Lens ◽  
Oxidative Stress Level ◽  
And Oxidative Stress ◽  
Cataract Patients

AbstractPurposeTo determine the effect of decorin on oxidative stress and apoptosis of human lens epithelial (HLE) cells under high glucose condition.MethodsHLE cell line (HLEB3) was incubated in normal glucose (5.5 mM) or high glucose (60 mM) medium. Decorin (50 nM) was applied 2 hours before high glucose medium was added. Apoptosis detection was executed by flow cytometry and western blotting (analysis of bcl-2 and bax). Oxidative stress level was measured by the generation of reactive oxygen species (ROS), glutathione peroxidase (GSH) and superoxide dismutase (SOD). P38 mitogen-activated protein kinase (MAPK) phosphorylation, the expression of p22phox of HLE cells and human lens anterior capsules were detected by western blotting. Small interfering RNA transfection to p22phox and p38 MAPK was also carried out on HLEB3.ResultsHigh glucose caused HLE cells oxidative stress and apoptosis exhibiting the increase of apoptotic cells and ROS production and decrease of bcl-2/bax ratio, GSH/GSSG ration and SOD activity. P22phox and phospho-p38 MAPK were upregulated in high glucose treated HLEB3 cells. Knocking down p22phox or p38 by siRNAs can reduce high glucose induced cell apoptosis and oxidative stress level. Silencing p22phox by siRNA can downregulate p38 MAPK activation. Decorin can inhibit the apoptosis, oxidative stress level and the induction of p22phox and p-p38 of HLEB3 induced by high glucose. Furthermore, the expression of p22phox and p38 were found significantly increased in lens anterior capsules of diabetic cataract patients compared to that of normal age-related cataract patients.ConclusionsResults showed that p22phox-p38 pathway may be particepated in high glucose induced lens epithelial cell injury, decorin may inhibit the high glucose induced apoptosis and oxidative stress injury by suppressing this pathway in part.

Asprosin and Oxidative Stress Level in COVID-19 Patients

2022 ◽  
Vol 68 (01/2022) ◽  
Author(s):  
E. Seyhanli ◽  
Ismail Koyuncu ◽  
I. Yasak ◽  
H. Demir ◽  
Ebru Temiz
Keyword(s):  
Oxidative Stress ◽  
Stress Level ◽  
Oxidative Stress Level ◽  
And Oxidative Stress

scholarly journals SUMOylation Evoked by Oxidative Stress Reduced Lens Epithelial Cell Antioxidant Functions by Increasing the Stability and Transcription of TP53INP1 in Age-Related Cataracts

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Bo Lu ◽  
Ian T. Christensen ◽  
Tao Yu ◽  
Chunxia Wang ◽  
Qichang Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Epithelial Cell ◽  
Cell Injury ◽  
Lens Epithelial Cell ◽  
Human Lens ◽  
Human Lens Epithelial Cell ◽  
Age Related ◽  
The Stability

Oxidative stress plays an important role in the pathogenesis of cataracts. Small ubiquitin-like modifier (SUMO) proteins have great effects on cell stress response. Previous studies have shown that TP53INP1 can arrest cell growth and induce apoptosis by modulating p53 transcriptional activity and that both TP53INP1 and p53 are substrates of SUMOylation. However, no previous research has studied the effect of SUMOylation on the oxidative stress response in cataracts. This is the first study to investigate the effect of SUMOylation of TP53INP1 in oxidative stress-induced lens epithelial cell injury and age-related cataract formation. We found that the oxidative stress-induced endogenous SUMOylation of TP53INP1 promoted human lens epithelial cell (holed) apoptosis and regulated hLEC antioxidant effects by increasing the stability and transcription of TP53INP1 in age-related cataracts. SUMO-1, SUMOylation, and TP53INP1 were upregulated in lens tissues affected by age-related cataracts. A SUMO-1-specific protease, SENP1, acted as an oxidative stress-sensitive target gene in hLECs. This study identified for the first time that TP53INP1 can be SUMOylated in vivo, that the SUMOylation of TP53INP1 is induced by oxidative stress, and that SUMOylation/deSUMOylation can affect the stability and transcription of TP53INP1 in hLECs.

scholarly journals Blood lead level modifies the association between dietary antioxidants and oxidative stress in an urban adult population

2012 ◽  
Vol 109 (1) ◽  
pp. 148-154 ◽  
Author(s):  
Yun-Chul Hong ◽  
Se-Young Oh ◽  
Sung-Ok Kwon ◽  
Min-Seon Park ◽  
Ho Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Level ◽  
Geometric Mean ◽  
Lead Level ◽  
Blood Lead ◽  
Oxidative Stress Marker ◽  
Dietary Intakes ◽  
Dietary Antioxidants ◽  
Oxidative Stress Level ◽  
And Oxidative Stress

Oxidative stress may be affected by lead exposure as well as antioxidants, yet little is known about the interaction between dietary antioxidants and blood lead levels (BLL) on oxidative stress level. We investigated the interaction between dietary antioxidants and BLL on oxidative stress level. As part of the Biomarker Monitoring for Environmental Health conducted in Seoul and Incheon, Korea, between April and December 2005, we analysed data from 683 adults (female = 47·4 %, mean age 51·4 (sd 8·4) years) who had complete measures on BLL, dietary intakes and oxidative stress marker (urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG)). Dietary intakes were assessed by a validated semi-quantitative FFQ, BLL was measured using atomic absorption spectrophotometry, and 8-OHdG by ELISA. Multivariate linear regression analyses were used to evaluate the influence of BLL on the association between dietary antioxidants and 8-OHdG. Geometric means of BLL and 8-OHdG concentrations were 4·1 (sd 1·5) μg/dl and 5·4 (sd 1·9) μg/g creatinine, respectively. Increases of vitamins C and E were significantly associated with the decrease of log10 8-OHdG in the adults from the lowest quartile of the BLL group ( ≤ 3·18 μg/dl, geometric mean = 2·36 μg/dl) than those of the highest quartile BLL group (>5·36 μg/dl, geometric mean = 6·78 μg/dl). Regarding antioxidant-related foods, vegetables excluding kimchi showed a higher inverse relationship with 8-OHdG in the lowest quartile BLL group than the highest group. These findings suggest a rationale for lowering the BLL and increasing the intake of dietary antioxidants in the urban population in Korea.

scholarly journals Yeast Fermentate Prebiotic Ameliorates Allergic Asthma, Associating with Inhibiting Inflammation and Reducing Oxidative Stress Level through Suppressing Autophagy

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Subo Gong ◽  
Xiaoying Ji ◽  
Jing Su ◽  
Yina Wang ◽  
Xianghong Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Tight Junction ◽  
Allergic Asthma ◽  
Signaling Pathway ◽  
Stress Level ◽  
Bacterial Species ◽  
Allergic Inflammation ◽  
Asthma Model ◽  
Oxidative Stress Level ◽  
And Oxidative Stress

Background and Purpose. Allergic asthma, a respiratory disease with high morbidity and mortality, is reported to be related to the airway allergic inflammation and autophagy-induced oxidative stress. Although the therapeutic effects of fermentate prebiotic (YFP) on allergic asthma have been widely claimed, the underlying mechanism is still unclear. This study is aimed at investigating the possible mechanism for the antiasthma property of YFP in a mouse model. Methods. Ovalbumin was used to induce allergic asthma following administration of YFP for one week in mice, to collect the lung tissues, bronchoalveolar lavage fluid (BLFA), and feces. The pathological state, tight-junction proteins, inflammatory and oxidative stress-associated biomarkers, and TLRs/NF-κB signaling pathway of the lung tissues were evaluated by HE staining, immunofluorescence, ELISA, and WB, separately. RT-PCR was used to test oxidative stress-associated genes. Leukocyte counts of BLFA and intestinal microbiota were also analyzed using a hemocytometer and 16S rDNA-sequencing, separately. Result. YFP ameliorated the lung injury of the mouse asthma model by inhibiting peribronchial and perivascular infiltrations of eosinophils and increasing tight-junction protein expression. YFP inhibited the decrease in the number of BALF leukocytes and expression of inflammatory-related genes and reversed OVA-induced TLRs/NF-κB signaling pathway activation. YFP ameliorated the level of oxidative stress in the lung of the mouse asthma model by inhibiting MDA and promoting the protein level of GSH-PX, SOD, CAT, and oxidative-related genes. ATG5, Beclin1, and LC3BII/I were significantly upregulated in asthma mice, which were greatly suppressed by the introduction of YFP, indicating that YFP ameliorated the autophagy in the lung of the mouse asthma model. Lastly, the distribution of bacterial species was slightly changed by YFP in asthma mice, with a significant difference in the relative abundance of 6 major bacterial species between the asthma and YFP groups. Conclusion. Our research showed that YFP might exert antiasthmatic effects by inhibiting airway allergic inflammation and oxidative stress level through suppressing autophagy.

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