Low Concentration Ethanol Prevents Oxidative Stress- Induced Cardiac Cells Injury Under HyperglycemicConditions by Inhibiting the SAPK/JNK Signaling Pathway and ROS Generation

2021 ◽  
Vol 7 (4) ◽  
Author(s):  
Tian Y ◽  
◽  
Tian W ◽  
Bai Y ◽  
Zhang A ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Fluorescence Intensity ◽  
Cardiac Cells ◽  
Ros Generation ◽  
Intensity Increase ◽  
H9c2 Cells ◽  
Jnk Signaling ◽  
Mitochondrial Injury ◽  
Jnk Signaling Pathway

The purpose of this study was to determine the effects and mechanisms of ethanol on oxidative stress-induced cardiac H9c2 cells mitochondrial injury under hyperglycemic conditions. Under hyperglycemic conditions, ethanol pretreatment (10-100 μM) prevented H2O2-induced mitochondria swelling, as well as decreased cell viability and Respiratory Control Ratio (RCR) in the H9c2 cells. It also prevented TMRE fluorescence intensity loss and DCF fluorescence intensity increase under hyperglycemic conditions. These effects of ethanol were reversed by the SAPK/JNK agonist, anisomycin. Finally, treatment of H9c2 cells with 33mM glucose significantly enhanced Akt and ERK phosphorylation, which was not affected by ethanol. However, ethanol decreased the phosphorylation of SAPK/JNK under hyperglycemic conditions. Collectively, these findings indicate that under hyperglycemic conditions, that ethanol prevents oxidative stress-induced mitochondrial injury in cardiac H9c2 cells by preventing ROS generation via inhibiting the SAPK/JNK signaling pathway.

Aluminum Induces Osteoblast Apoptosis Through the Oxidative Stress-Mediated JNK Signaling Pathway

2012 ◽  
Vol 150 (1-3) ◽  
pp. 502-508 ◽  
Author(s):  
Xinwei Li ◽  
Yanfei Han ◽  
Yuan Guan ◽  
Liang Zhang ◽  
Chongsheng Bai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway ◽  
Osteoblast Apoptosis

Role and Mechanisms of Probiotics in Regulating the ROS/JNK Signaling Pathway in the Pathogenesis of Nonalcoholic Fatty Liver Disease.

2021 ◽  
Author(s):  
HuiYuan Xu ◽  
LeiLei Yang ◽  
YuMei Huang ◽  
ChangPing Li
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Signaling Pathway ◽  
Fatty Liver Disease ◽  
Intestinal Barrier ◽  
Jnk Signaling ◽  
Nonalcoholic Fatty Liver ◽  
Jnk Signaling Pathway

Abstract This study was aimed to investigate the impact of probiotics on regulating the ROS/JNK signaling pathway their underlying mechanism of action in the treatment of nonalcoholic fatty liver disease. For this purpose, male C57BL/6 mice were randomly divided into three groups: control, probiotics, and model groups. Methionine and choline deficiency (MCD) diets were fed for four weeks to establish a NAFLD mouse model. Serum levels of ALT, AST, TC, and TG were detected. Moreover, the pathological changes of the liver and ileum tissues were observed by hematoxylin and eosin (H&E) staining, and the content of reactive oxygen species (ROS) in liver tissues was determined. In addition, the levels of D-lactic acid and plasma and small intestine diamine oxidase were measured to evaluate the effects of probiotics on the intestinal tract of NAFLD mice. The expression levels of p-JNK, Bax, and Caspase-3 were established to analyze the regulatory mechanism of probiotics on the JNK signaling pathway. We found that probiotics improve liver function, repair intestinal barrier and significantly suppressed oxidative stress, JNK phosphorylation. Moreover, the application of probiotics regulated the expression of signaling pathway-related proteins and promoted the intestinal barrier function repair and decreased intestinal permeability. The data above suggest that probiotics alleviate NAFLD, whose mechanism might be associated with the regulation of ROS/JNK signaling pathway and the suppression of oxidative stress and apoptosis.

scholarly journals Dexmedetomidine Ameliorates Acute Stress-Induced Kidney Injury by Attenuating Oxidative Stress and Apoptosis through Inhibition of the ROS/JNK Signaling Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Yongping Chen ◽  
Xiujing Feng ◽  
Xueyuan Hu ◽  
Jichen Sha ◽  
Bei Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Acute Stress ◽  
Death Receptor ◽  
Kidney Injury ◽  
Jnk Pathway ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway

Acute stress induces tissue damage through excessive oxidative stress. Dexmedetomidine (DEX) reportedly has an antioxidant effect. However, protective roles and related potential molecular mechanisms of DEX against kidney injury induced by acute stress are unknown. Herein, rats were forced to swim 15 min followed by restraint stress for 3 h with/without DEX (30 μg/kg). Successful model establishment was validated by an open-field test. Assessment of renal function (creatinine, urea nitrogen), histopathology, oxidative stress (malondialdehyde, glutathione, and superoxide dismutase), and apoptosis (transferase-mediated dUTP nick end labeling) was performed. Localization of apoptosis was determined by immunohistochemistry of cleaved caspase 3 protein. In addition, key proteins of the death receptor-mediated pathway, mitochondrial pathway, endoplasmic reticulum stress (ERS) pathway, and ROS/JNK signaling pathway were measured by Western blot. We found that DEX significantly improved renal dysfunction, ameliorated kidney injury, reduced oxidative stress, and alleviated apoptosis. DEX also inhibited the release of norepinephrine (NE), decreased the production of reactive oxygen species (ROS), and inhibited JNK phosphorylation. Additionally, DEX downregulated the expression of Bax, cytochrome C, cleaved caspase 9, and cleaved caspase 3 proteins in mitochondria-dependent pathways. In summary, DEX protects against acute stress-induced kidney injury in rats by reducing oxidative stress and apoptosis via inhibition of the ROS/JNK pathway.

scholarly journals Myc is involved in Genistein protecting against LPS-induced myocarditis in vitro through mediating MAPK/JNK signaling pathway

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Chunhua Huang ◽  
Yan Zhang ◽  
Hongli Qi ◽  
Xintan Xu ◽  
Lin Yang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Mapk Pathway ◽  
Enrichment Analysis ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Effects ◽  
H9c2 Cells ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway

Abstract Background: Genistein is widely used as a pharmacological compound as well as a food additive. However, the pharmaceutical effects of Genistein on myocarditis and its potential mechanisms have not been studied in detail. Methods: H9c2 cells were continuously stimulated by lipopolysaccharide (LPS) for 12 h to simulate the in vitro model of myocarditis injury. DrugBank, String, and GEO dataset were used to investigate specific genes that interacting with Genistein. KEGG and GO enrichment analysis were employed to explore Myc-related signaling pathways. Biological behaviors of H9c2 cells were observed with the support of cell counting kit-8, MTT and flow cytometry. Expression levels of cytokines including TNF-α and ILs were evaluated by enzyme-linked immunosorbent assay. Western blot was applied to detect the expression of Myc and MAPK pathway related proteins. Results: Genistein alleviated the damage of H9c2 cells subjected to LPS from the perspective of elevating cells growth ability, and inhibiting cells apoptosis and inflammatory response. Through bioinformatics analysis, we identified Myc as the potential target of Genistein in myocarditis, and MAPK as the signaling pathway. Significantly, Myc was highly up-regulated in myocarditis samples. More importantly, by performing biological experiments, we discovered that Genistein relieved H9c2 cells apoptosis and inflammatory reaction which caused by LPS stimulation through inhibiting Myc expression. Additionally, the marked augmentation of p-P38 MAPK and p-JNK expression in LPS-induced cardiomyocyte model were blocked by Genistein and si-Myc. Conclusions: Our research revealed that Myc mediated the protective effects of Genistein on H9c2 cells damage caused by LPS partly through modulation of MAPK/JNK signaling pathway.

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