Repeated exposure to far infrared ray attenuates acute restraint stress in mice via inhibition of JAK2/STAT3 signaling pathway by induction of glutathione peroxidase-1

2016 ◽  
Vol 94 ◽  
pp. 9-22 ◽  
Author(s):  
Thai-Ha Nguyen Tran ◽  
Huynh Nhu Mai ◽  
Eun-Joo Shin ◽  
Yunsung Nam ◽  
Bao Trong Nguyen ◽  
...  
Keyword(s):  
Glutathione Peroxidase ◽  
Signaling Pathway ◽  
Restraint Stress ◽  
Far Infrared ◽  
Repeated Exposure ◽  
Glutathione Peroxidase 1 ◽  
Stat3 Signaling ◽  
Acute Restraint Stress ◽  
Stat3 Signaling Pathway ◽  
Far Infrared Ray

Rhein Activates Janus Protein Tyrosine Kinase2/Signal Transducer and Transcription Activation Factor3 Reduces Mitochondrial Oxidative Damage Caused by Myocardial Ischemia/Reperfusion Injury

2021 ◽  
Vol 11 (1) ◽  
pp. 89-98
Author(s):  
Jianxian Xiong ◽  
Dongmin Yu ◽  
Wentong Li ◽  
Xiaowei Wang
Keyword(s):  
Myocardial Ischemia ◽  
Glutathione Peroxidase ◽  
Signaling Pathway ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Cells ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Background: Rhein is a kind of lipophilic anthraquinone widely existing in herbal medicine. Here we aim to investigate whether Rhein can reduce the degree of myocardial ischemia/reperfusion injury and inhibit the development of oxidative stress, and elucidate the molecular mechanism of Rhein in protecting myocardial cells. Methods: The anti-oxidation and anti-apoptosis effects of Rhein were studied by using the primary myocardial cells of ischemia/reperfusion rat as the model of myocardial injury. Cell viability was detected by MTT, The level of LDH and CK-MB released by cardiomyocytes was measured by Colorimetric assay. The ROS was observed under microscope and the level of catalase and glutathione peroxidase were detected by enzymatic methods. The JAK2/STAT3 signaling pathway mediated by Rhein was observed by Western blot. Results: Compared with that of the SIR group, cell viability in the SIR and Rhein co-treatment groups increased significantly (P < 0.001), the release of LDH and CK-MB decreased, the positive rate of ROS in cardiomyocytes decreased, and the concentration of catalase and glutathione peroxidase increased significantly (P < 0.001). Besides, Rhein can activate JAK2/STAT3 signaling pathway. JAK2 siRNA can inhibit the JAK2/STAT3 signaling mediated by Rhein. The addition of Rhein can significantly increase the activity of mitochondrial superoxide dismutase (SOD) and reduce the MDA, which indicates that the oxidative damage of mitochondria induced by Rhein was significantly weakened. The mitochondrial functional changes induced by Rhein can be reversed by JAK2 siRNA. Conclusion: Our study shows that Rhein can reduce ROS in cardiomyocytes by JAK2/STAT3 signaling pathway activation, and effectively inhibit the apoptosis of cardiomyocytes, thus having a direct protective effect on cardiomyocytes under SIR.

scholarly journals The glutathione peroxidase 8 (GPX8)/IL-6/STAT3 axis is essential in maintaining an aggressive breast cancer phenotype

2020 ◽  
Vol 117 (35) ◽  
pp. 21420-21431
Author(s):  
Anees Khatib ◽  
Balakrishnan Solaimuthu ◽  
Michal Ben Yosef ◽  
Areej Abu Rmaileh ◽  
Mayur Tanna ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Glutathione Peroxidase ◽  
Signaling Pathway ◽  
Building Blocks ◽  
Metabolic Reprogramming ◽  
Mesenchymal Transition ◽  
Stat3 Signaling ◽  
Tumor Plasticity ◽  
Stat3 Signaling Pathway ◽  
Cancer Aggressiveness

One of the emerging hallmarks of cancer illustrates the importance of metabolic reprogramming, necessary to synthesize the building blocks required to fulfill the high demands of rapidly proliferating cells. However, the proliferation-independent instructive role of metabolic enzymes in tumor plasticity is still unclear. Here, we provide evidence that glutathione peroxidase 8 (GPX8), a poorly characterized enzyme that resides in the endoplasmic reticulum, is an essential regulator of tumor aggressiveness. We found that GPX8 expression was induced by the epithelial–mesenchymal transition (EMT) program. Moreover, in breast cancer patients, GPX8 expression significantly correlated with known mesenchymal markers and poor prognosis. Strikingly, GPX8 knockout in mesenchymal-like cells (MDA-MB-231) resulted in an epithelial-like morphology, down-regulation of EMT characteristics, and loss of cancer stemness features. In addition, GPX8 knockout significantly delayed tumor initiation and decreased its growth rate in mice. We found that these GPX8 loss-dependent phenotypes were accompanied by the repression of crucial autocrine factors, in particular, interleukin-6 (IL-6). In these cells, IL-6 bound to the soluble receptor (sIL6R), stimulating the JAK/STAT3 signaling pathway by IL-6trans-signaling mechanisms, so promoting cancer aggressiveness. We observed that in GPX8 knockout cells, this signaling mechanism was impaired as sIL6R failed to activate the JAK/STAT3 signaling pathway. Altogether, we present the GPX8/IL-6/STAT3 axis as a metabolic-inflammatory pathway that acts as a robust regulator of cancer cell aggressiveness.

scholarly journals Mechanism of miR-218-5p in autophagy, apoptosis and oxidative stress in rheumatoid arthritis synovial fibroblasts is mediated by KLF9 and JAK/STAT3 pathways

2021 ◽  
pp. jim-2020-001437
Author(s):  
Ming Chen ◽  
Minghui Li ◽  
Na Zhang ◽  
Wenwen Sun ◽  
Hui Wang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Signaling Pathway ◽  
Synovial Tissue ◽  
Synovial Fibroblasts ◽  
Reverse Transcription Pcr ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Interfering Rna ◽  
And Oxidative Stress

This study was aimed to investigate the effects of miR-218-5p on the proliferation, apoptosis, autophagy, and oxidative stress of rheumatoid arthritis synovial fibroblasts (RASFs), and the related mechanisms. Quantitative reverse transcription–PCR showed that the expression of miR-218-5p in rheumatoid arthritis synovial tissue was significantly higher than that in healthy synovial tissue. Compared with healthy synovial fibroblasts, miR-218-5p expression was obviously upregulated in RASFs, while KLF9 protein expression was markedly downregulated. Mechanistically, miR-218-5p could directly bind to the 3′ untranslated region of KLF9 to inhibit the expression of KLF9. Additionally, transfection of miR-218-5p small interfering RNA (siRNA) inhibited the proliferation but promoted apoptosis and autophagy of RASFs. Simultaneously, miR-218-5p silencing reduced reactive oxygen species and malondialdehyde levels and increased superoxide dismutase and glutathione peroxidase activity to improve oxidative stress in RASFs. More importantly, the introduction of KLF9 siRNA reversed the effects of miR-218-5p siRNA transfection on RASF proliferation, apoptosis, autophagy, and oxidative stress. What is more, silencing miR-218-5p inhibited the activation of JAK2/STAT3 signaling pathway by targeting KLF9. Collectively, knockdown of miR-218-5p could regulate the proliferation, apoptosis, autophagy and oxidative stress of RASFs by increasing the expression of KLF9 and inhibiting the activation of the JAK2/STAT3 signaling pathway, which may provide a potential target for the mechanism research of RA.

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