Molecular hydrogen protects mice against polymicrobial sepsis by ameliorating endothelial dysfunction via an Nrf2/HO-1 signaling pathway

2015 ◽  
Vol 28 (1) ◽  
pp. 643-654 ◽  
Author(s):  
Hongguang Chen ◽  
Keliang Xie ◽  
Huanzhi Han ◽  
Yuan Li ◽  
Lingling Liu ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Signaling Pathway ◽  
Molecular Hydrogen ◽  
Polymicrobial Sepsis

Paeonol protects against endoplasmic reticulum stress-induced endothelial dysfunction via AMPK/PPARδ signaling pathway

2016 ◽  
Vol 116 ◽  
pp. 51-62 ◽  
Author(s):  
Ker-Woon Choy ◽  
Mohd Rais Mustafa ◽  
Yeh Siang Lau ◽  
Jian Liu ◽  
Dharmani Murugan ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endothelial Dysfunction ◽  
Endoplasmic Reticulum Stress ◽  
Signaling Pathway

Astragaloside IV improves vascular endothelial dysfunction by inhibiting the TLR4/NF-κB signaling pathway

Life Sciences ◽  
2018 ◽  
Vol 209 ◽  
pp. 111-121 ◽  
Author(s):  
Bin Leng ◽  
Futian Tang ◽  
Meili Lu ◽  
Zhen Zhang ◽  
Hongxin Wang ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Signaling Pathway ◽  
Vascular Endothelial ◽  
Vascular Endothelial Dysfunction ◽  
Astragaloside Iv

scholarly journals Melatonin Attenuates ox-LDL-Induced Endothelial Dysfunction by Reducing ER Stress and Inhibiting JNK/Mff Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Peng Li ◽  
Changlian Xie ◽  
Jiankai Zhong ◽  
Zhongzhou Guo ◽  
Kai Guo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Mitochondrial Function ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Mitochondrial Ros ◽  
Er Homeostasis

Endothelial dysfunction, which is characterized by damage to the endoplasmic reticulum (ER) and mitochondria, is involved in a variety of cardiovascular disorders. Here, we explored whether mitochondrial damage and ER stress are associated with endothelial dysfunction. We also examined whether and how melatonin protects against oxidized low-density lipoprotein- (ox-LDL-) induced damage in endothelial cells. We found that CHOP, GRP78, and PERK expressions, which are indicative of ER stress, increased significantly in response to ox-LDL treatment. ox-LDL also induced mitochondrial dysfunction as evidenced by decreased mitochondrial membrane potential, increased mitochondrial ROS levels, and downregulation of mitochondrial protective factors. In addition, ox-LDL inhibited antioxidative processes, as evidenced by decreased antioxidative enzyme activity and reduced Nrf2/HO-1 expression. Melatonin clearly reduced ER stress and promoted mitochondrial function and antioxidative processes in the presence of ox-LDL. Molecular investigation revealed that ox-LDL activated the JNK/Mff signaling pathway, and melatonin blocked this effect. These results demonstrate that ox-LDL induces ER stress and mitochondrial dysfunction and activates the JNK/Mff signaling pathway, thereby contributing to endothelial dysfunction. Moreover, melatonin inhibited JNK/Mff signaling and sustained ER homeostasis and mitochondrial function, thereby protecting endothelial cells against ox-LDL-induced damage.

C1q/TNF–Related Protein-3 attenuates endothelial dysfunction in diabetic retinopathy via the Nitric Oxide signaling pathway

2020 ◽  
Author(s):  
Zheyi Yan ◽  
Xiaoming Cao ◽  
Chunfang Wang ◽  
Sha Liu ◽  
Lu Gan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Cell Death ◽  
Diabetic Retinopathy ◽  
Endothelial Dysfunction ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Apoptotic Cell ◽  
Related Protein

Abstract Background Diabetic retinopathy (DR) is a severe microvasculature complication of diabetes. Restoration of dysfunctional endothelial cells represents a promising approach to treatment of DR. It has been demonstrated that a number of CTRP (C1q/tumor necrosis factor-related protein) members improves vascular endothelial function of the aortic vasculature. However, the role of CTRPs in the treatment of DR remains largely unresolved. Therefore, the aim of this study was to determine whether members of the CTRP family improve diabetes-induced endothelial dysfunction of retinal vasculature, thus exhibiting a protective effect against diabetic injury of retina. Methods The vasoactivity of currently identified murine CTRP family members was assessed in vascular rings and the underlying molecular mechanisms elucidated in human retinal microvascular endothelial cells. We then mimicked diabetic retinopathy both in vitro and in vivo, after which they were treated with CTRP3, and the vasoactivity, apoptotic cell death and vascular leakage in the retina were evaluated. Discovery-drive approaches followed by cause-effect analysis were used to uncover the molecular mechanisms of CTRP3. Results Our results demonstrate that CTRP3, CTRP5, and CTRP9 exert vasorelaxant effects on macro- and micro-vessels, with CTRP3 being the most potent in micro-vessels. The effects of CTRP3 were found to be endothelium-dependent via the AdipoR1/AMPK/eNOS/Nitric Oxide (NO) pathway. In in vitro microvascular reactivity studies, CTRP3 successfully improved high glucose/high lipid-induced impairment of endothelium-dependent vasodilatation. Blockade of either AMPK or eNOS completely abolished the previously observed effects of CTRP3. In addition, in the murine diabetic retinopathy model, CTRP3 treatment increased endothelium-dependent relaxation and NO levels in microvessels, and inhibited apoptotic cell death and vascular leakage in the retina. Finally,blockade of NO synthesis completely abolished the effects of CTRP3 that had been measured previously. Conclusion Taken together, our findings reveal that the AdipoR1/AMPK/eNOS/NO signaling pathway, through which CTRP3 reverses endothelial dysfunction of the microvasculature by normalization of impaired vasodilatation, represents a novel intervention effective against diabetic injury of retina.

Cardio protective Effects of Eritoran during Polymicrobial Sepsis through Decreases of p38MAPK/NF-κB Signaling Pathway

2020 ◽  
Vol 106 (S1) ◽  
Author(s):  
Nasser Ghaly Yousif ◽  
Najah R Hadi ◽  
Qassim A Zigam ◽  
Ahmed N Altimimi
Keyword(s):  
Signaling Pathway ◽  
Polymicrobial Sepsis ◽  
Protective Effects
Sign in / Sign up

Export Citation Format

Share Document