scholarly journals Selenomethionine alleviates LPS-induced chicken myocardial inflammation by regulating the miR-128-3p-p38 MAPK axis and oxidative stress

Metallomics ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 54-64 ◽  
Author(s):  
Jing Liu ◽  
Shengchen Wang ◽  
Qiaojian Zhang ◽  
Xiaojing Li ◽  
Shiwen Xu
Keyword(s):  
Oxidative Stress ◽  
P38 Mapk ◽  
Myocardial Inflammation ◽  
Green Line ◽  
Yellow Line ◽  
And Oxidative Stress

The yellow line displays the promotion and the green line displays the inhibition. miR: microRNA; Se: selenium.

Inhibition of p38 MAPK improves intestinal disturbances and oxidative stress induced in a rabbit endotoxemia model

2009 ◽  
Vol 22 (5) ◽  
pp. 564-e123 ◽  
Author(s):  
S. Gonzalo ◽  
L. Grasa ◽  
M. P. Arruebo ◽  
M.á. Plaza ◽  
M. D. Murillo
Keyword(s):  
Oxidative Stress ◽  
P38 Mapk ◽  
Endotoxemia Model ◽  
And Oxidative Stress

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.

Thymoquinone and geraniol alleviate cisplatin-induced neurotoxicity in rats through downregulating the p38 MAPK/STAT-1 pathway and oxidative stress

Life Sciences ◽  
2019 ◽  
Vol 228 ◽  
pp. 145-151 ◽  
Author(s):  
Mohamed A. Kandeil ◽  
Mohamed O. Mahmoud ◽  
Abdel-Razik H. Abdel-Razik ◽  
Safaa B. Gomaa
Keyword(s):  
Oxidative Stress ◽  
P38 Mapk ◽  
And Oxidative Stress

scholarly journals Neferine induces p38 MAPK/JNK1/2 activation to modulate melanoma proliferation, apoptosis, and oxidative stress

2020 ◽  
Vol 8 (24) ◽  
pp. 1643-1643
Author(s):  
Jun Xie ◽  
Ming-Hui Chen ◽  
Chuan-Peng Ying ◽  
Ming-Yi Chen
Keyword(s):  
Oxidative Stress ◽  
P38 Mapk ◽  
And Oxidative Stress

Abstract 326: Cd36 Deficiency Reduces Obesity-associated Inflammation And Oxidative Stress In Heart

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Tahar Hajri ◽  
Mohamed Gharib ◽  
Thomas V Fungwe
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Glucose Uptake ◽  
Fatty Acid Oxidation ◽  
P38 Mapk ◽  
Acid Oxidation ◽  
Cd36 Deficiency ◽  
Anti Oxidant ◽  
The Impact ◽  
And Oxidative Stress

OBJECTIVE: Obesity is often associated with diabetes and cardiovascular diseases (CVD). Mounting evidence shows that diabetes is associated with structural and functional changes in the heart. CD36 protein is highly expressed in heart and regulates lipid utilization in cardiacmyocytes. In this paper, we investigated the impact of CD36 expression on obesity-associated inflammation and oxidative stress in heart. METHODS: Studies were conducted in control lean (WT), obese leptin deficient (Lep Ob/Ob ) and leptin deficient-CD36 null (Lep Ob/Ob -CD36 -/- ) mice. To examine obesity-associated insulin resistance, glucose uptake and insulin signaling were examined in adult mouse hearts. Presence of macrophages in heart was examined with immunohistochemisty. Oxidative stress makers and activity of anti-oxidant enzymes were measured in hearts. To evaluate substrate utilization, glucose and fatty acid oxidation was tested in primary cultures of ventricular myocytes. Finally, the activity of pro-inflammatory kinases p38 mitogen-activated protein kinases (p38-MAPK), c-Jun NH2-terminal kinases (JNK) were examined in cardiacmyocytes challenged with palmitate. RESULTS: In Lep Ob/Ob , glucose uptake and oxidation in heart was lower than lean WT mice, while cardiac FA oxidation was strongly higher. Silencing CD36 in Lep Ob/Ob mouse markedly improved insulin sensitivity and glucose uptake in heart, but resulted in marked reduction of FA oxidation. Immunostaining of heart sections with macrophage specific antibody F4/80 showed that macrophage content was higher in myocardium of Lep Ob/Ob mice than Lep Ob/Ob -CD36 -/- mice. Moreover, oxidative stress markers, isoprostanes and reactive oxygen species, and expression of pro-inflammatory cytokines were higher in hearts of Lep Ob/Ob than Lep Ob/Ob -CD36-/- mice, although the activities of anti-oxidant enzymes were comparable. Chronic overload of Lep Ob/Ob cardiac myocyte with palmitate strongly induced the activity of JNK and p38-MAPK, but was less effective in Lep Ob/Ob -CD36 -/- cardiac myocytes. CONCLUSIONS: These results show that CD36 deficiency induced a significant reduction of obesity-associated oxidative stress and inflammation in heart in parallel to a drop in fatty acid oxidation.

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