Asset Details
Do you wish to reserve the book?
Protective effect of Pinacidil on hypoxic-reoxygenated cardiomyocytes in vitro and in vivo via HIF-1α/HRE pathway
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Protective effect of Pinacidil on hypoxic-reoxygenated cardiomyocytes in vitro and in vivo via HIF-1α/HRE pathway
Do you wish to request the book?
Protective effect of Pinacidil on hypoxic-reoxygenated cardiomyocytes in vitro and in vivo via HIF-1α/HRE pathway
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Protective effect of Pinacidil on hypoxic-reoxygenated cardiomyocytes in vitro and in vivo via HIF-1α/HRE pathway
2025
Overview
Cardiomyocyte hypoxia-reoxygenation (HR) is considered as a major cause of heart failure. Pinacidil is a classic ATP sensitive potassium channel opener and plays a crucial role in cardiomyocyte HR injuries. However, the specific mechanism is poorly understood. We established HR rat model and introduced 5-Hydroxydecanoate (5-HD), N-(2-Mercaptopropionyl)-glycine (MPG), and Dimethylethylenediylglycine (DMOG) to investigate the protection of Pinacidil (P) on cardiomyocyte. HE staining, electron microscopy and JC-1 staining were used to observe mitochondrial structure and mitochondrial membrane potential (MMP). Reactive oxygen species (ROS), hypoxia-inducible factor-1α (HIF-1α), vascular endothelial growth factor A (VEGF-A), heme oxygenase-1 (HO-1), and induced nitric oxide synthase (iNOS) were analyzed in this study. Network pharmacology analysis and auto-docking were used to predict the possible target of Pinadicil under cardiomyocyte HR condition. The integrity of mitochondrial structure and MMP were effectively promoted in P and MPG+DMOG + P groups. ROS was significantly increased after HR, treatment with P or MPG+DMOG + P, the content of ROS was increased. The expressions of HIF-1α, VEGF-A, HO-1 and iNOS were significantly increased in P and MPG+DMOG + P groups compared with HR group. Docking results confirmed that prolyl hydroxylase (PHD) was the most possible target for unsaturated binding with Pinacidil guanidine. Altogether, these data indicate that Pinacidil up-regulated and activated HIF-1α protein to protect caridomyocytes against HR injuries and the mechanism may be related to Pinacidil guanidine binding to PHD.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Binding
/ Glycine
/ Heart
/ Heme oxygenase (decyclizing)
/ Heme Oxygenase-1 - metabolism
/ Hypoxia
/ Hypoxia-Inducible Factor 1, alpha Subunit - metabolism
/ Injuries
/ Ischemia
/ Male
/ Medicine and Health Sciences
/ Membrane Potential, Mitochondrial - drug effects
/ Myocytes, Cardiac - drug effects
/ Myocytes, Cardiac - metabolism
/ Nitric Oxide Synthase Type II - metabolism
/ Rats
/ Reactive Oxygen Species - metabolism
/ Research and Analysis Methods
/ Signal Transduction - drug effects
/ Staining
