98%
921
2 minutes
20
Lung ischemia-reperfusion (I/R) injury represents an inevitable complication in lung transplantation, characterized by the excessive production of oxygen free radicals and toxic substances. Dexmedetomidine (DEX), a widely used anesthetic agent, has been shown to significantly elevate glutathione (GSH) levels, thereby conferring protection against copper influx. This study investigates the protective mechanisms of DEX in lung I/R injury, with a particular focus on cuproptosis. Utilizing a rat I/R model established by clamping the left hilum of lung for 90 min followed by 120 min of reperfusion, we examined the effects of DEX on lung injury scores, GSH content, and the expression of key proteins involved in cuproptosis. In conclusion, cuproptosis is implicated in pulmonary I/R injury, and the protective effect of DEX against lung I/R injury is partly mediated by inhibition of cuproptosis.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11996775 | PMC |
http://dx.doi.org/10.3389/fphar.2025.1562535 | DOI Listing |
J Ethnopharmacol
September 2025
Department of Traditional Chinese Medicine, Qingdao Municipal Hospital, Qingdao, China. Electronic address:
Ethnopharmacological Relevance: Acute kidney injury (AKI) is a growing worldwide health concern. Danggui Shaoyao San (DGSYS) was an frequently-used representative prescription to "promote blood and water and harmonize the body" in traditional Chinese medicine, and its underlying mechanism against AKI remains to be elucidated.
Aim Of The Study: To investigate the protective effect and potential molecular mechanism of DGSYS in alleviating AKI by network pharmacology and experiment validation.
Eur J Pharmacol
September 2025
Department of Cardiovascular Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, China. Electronic address:
Purpose: Ischemia-reperfusion injury remains a major problem following myocardial infarction. Alpinetin (ALPT) has been reported to exhibit cardioprotective effects as well as resistance to ischemia-reperfusion injury. However, its role and mechanism during myocardial ischemia-reperfusion injury are unknown.
View Article and Find Full Text PDFFree Radic Biol Med
September 2025
Laboratory of Clinical and Experimental Pathology, Xuzhou Medical University, Xuzhou, China; National Demonstration Center for Experimental Basic Medical Science Education, Xuzhou Medical University, Xuzhou China. Electronic address:
Elevated H3K27me3 levels during cerebral I/R injury exacerbate neuronal damage through oxidative stress, but the underlying mechanism remains to be elucidated. We hypothesized that reduced H3K27me3 confers protection by modulating FOXP1 expression. Employing multifaceted approaches, we demonstrate that H3K27me3 reduction in vivo and in vitro enhances lipid metabolism and rescues oxygen-glucose deprivation (OGD)-induced mitochondrial morphological abnormalities and functional deficits.
View Article and Find Full Text PDFTranspl Immunol
September 2025
Department of Cardiovascular Medicine, Tianjin Medical University General Hospital, Tianjin City 300000, PR China. Electronic address:
Background: Myocardial ischemia/reperfusion (I/R) injury is a common cause of death. FXYD domain-containing ion transport regulator-5 (Fxyd5) is a type I membrane protein that plays a significant role in mediating cellular functions. However, the expression and function of Fxyd5 in myocardial I/R injury remain unclear.
View Article and Find Full Text PDFPharmacol Rep
September 2025
The First Affiliated Hospital of Xinjiang Medical University, Xinjiang Medical University, Wulumuqi, Xinjiang, 830011, China.