scholarly journals Propofol Induces Cardioprotection Against Ischemia-Reperfusion Injury via Suppression of Transient Receptor Potential Vanilloid 4 Channel

2019 ◽  
Vol 10 ◽  
Author(s):  
Binbin Wang ◽  
Qiongfeng Wu ◽  
Jie Liao ◽  
Shaoshao Zhang ◽  
Huixia Liu ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Transient Receptor Potential ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Transient Receptor

A Review on Potential Involvement of TRPV1 Channels in Ischemia–Reperfusion Injury

2017 ◽  
Vol 23 (1) ◽  
pp. 38-45 ◽  
Author(s):  
Puneet Kaur Randhawa ◽  
Amteshwar Singh Jaggi
Keyword(s):  
Reperfusion Injury ◽  
Inflammatory Cytokines ◽  
Transient Receptor Potential ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Channel Activation ◽  
Trpv1 Channels ◽  
Transient Receptor

Besides functioning as thermosensors, transient receptor potential vanilloid 1 (TRPV1) channels play a pivotal role in ischemia–reperfusion injury. Transient receptor potential vanilloid 1 channel activation attenuates ischemia–reperfusion-induced injury in various organs including the heart, lungs, kidneys, and the brain. Transient receptor potential vanilloid 1 channels are expressed on the sensory neurons innervating the myocardium, ventricles of the heart, epicardial surface of the heart, endothelial cells, and the vascular smooth muscle cells. During ischemic conditions, activation of TRPV1 channels on the perivascular nerves stimulates the release of calcitonin gene-related peptide and substance P to produce cardioprotection. Furthermore, TRPV1 channel activation reduces the generation of free radicals and inflammatory cytokines, inhibits neutrophil infiltration, and enhances the production of anti-inflammatory cytokines to reduce ischemia–reperfusion-induced tissue injury. The present review describes the potential involvement of TRPV1 channels and the signaling cascade in attenuating ischemia–reperfusion injury in various organs.

scholarly journals Products of oxidative stress and transient receptor potential ankyrin A1 expression in the brainstem after lung ischemia–reperfusion injury

2019 ◽  
Vol 9 (3) ◽  
pp. 204589401986516 ◽  
Author(s):  
Xiaoying Gu ◽  
Yu Nan ◽  
Xiaochuan Pang ◽  
Wenwen Zhang ◽  
Jian Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Transient Receptor Potential ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Receptor Potential ◽  
Antioxidant Response ◽  
Solitary Tract ◽  
Transient Receptor Potential A1 ◽  
Transient Receptor

Lung ischemia–reperfusion injury is a common clinical concern. As the injury occurs, the pulmonary afferent nerves play a key role in regulating respiratory functions under pathophysiological conditions. The present study was to examine products of oxidative stress and expression of transient receptor potential A1 in the commissural nucleus of the solitary tract after lung ischemia–reperfusion injury; and further to determine molecular mediators linking to activation of oxidative stress and transient receptor potential ankyrin A1. A rat model of lung ischemia–reperfusion injury was used. Enzyme-linked immunosorbent assay and western blot analysis were employed to examine products of oxidative stress (i.e. 8-isoprostaglandin F2α and 8-hydroxy-2′-deoxyguanosine), and expression of transient receptor potential A1, Nrf2-antioxidant response element, and NADPH oxidase. 8-isoprostaglandin F2α and 8-hydroxy-2′-deoxyguanosine were amplified in the commissural nucleus of the solitary tract of lung ischemia–reperfusion injury rats, accompanied with downregulation of Nrf2-antioxidant response element, and upregulation of NOX4 and transient receptor potential A1. Blocking NADPH oxidase (subtype NOX4) decreased products of oxidative stress in the commissural nucleus of the solitary tract and attenuated upregulation of transient receptor potential A1 induced by lung ischemia–reperfusion injury. Our data revealed specific signaling pathways by which lung ischemia–reperfusion injury impairs Nrf2-antioxidant response and activates oxidative stress in the brainstem thereby leading to amplification of transient receptor potential A1 receptor likely via products of oxidative stress. Data suggest the abnormalities in the pulmonary afferent signals at the brainstem level which is likely to affect respiratory functions as lung ischemia–reperfusion injury occurs.

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