Kv channels represent new important targets for the control of cancer growth and a better understanding of their regulating pathways in cancer cells is necessary to develop therapeutic strategies. In this study, we have addressed the putative modulation of Kv by MAP kinases through a pharmacological approach. We have found that the commonly used JNK inhibitor SP600125 strongly inhibits Kv channels through a JNK-independent pathway, likely interacting directly with the channels at the external side of the membrane. Our results indicate that the use of this compound may produce misleading conclusions for the role of JNK in cell cycle.
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http://dx.doi.org/10.1016/j.bbrc.2007.12.027 | DOI Listing |
CNS Neurosci Ther
January 2025
Qingshan Lake Science and Technology Innovation Center, Hangzhou Medical College, Hangzhou, China.
Background: Ischemic stroke is a prevalent and life-threatening cerebrovascular disease that is challenging to treat and associated with a poor prognosis. Astragaloside IV (AS-IV), a primary bioactive component of Astragali radix, has demonstrated neuroprotective benefits in previous studies. This study aimed to explore the mechanisms through which AS-IV may treat cerebral ischemia-reperfusion injury (CIRI).
View Article and Find Full Text PDFCell Death Dis
January 2025
State Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, Department of Pulmonary and Critical Care Medicine, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, 510120, China.
Immune checkpoint inhibitors (ICIs) have significant therapeutic effects but can also cause fatal lung injury. However, the lack of mouse animal models of ICI-related lung injury (ICI-LI) has limited the in-depth exploration of its pathogenesis. In clinical practice, underlying lung diseases increase the risk of lung injury.
View Article and Find Full Text PDFInt J Med Sci
January 2025
Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
This study aimed to investigate the involvement of macrophage ferroptosis in chronic apical periodontitis (CAP) and determine if blocking JNK/JUN/NCOA4 axis could alleviate CAP by regulating macrophage ferroptosis. Firstly, the models of apical periodontitis (AP) and models of CAP, including clinical specimens and rats' periapical lesions, were utilized to investigate the role of macrophage ferroptosis in CAP by detecting the ferroptosis related factors. The activation of the JNK/JUN/NCOA4 axis was observed in CAP models.
View Article and Find Full Text PDFNeurochem Int
December 2024
Master and PhD Programs in Pharmacology and Toxicology, School of Medicine, Tzu Chi University, Hualien, 970, Taiwan; Department of Pharmacology, School of Medicine, Tzu Chi University, Hualien, 970, Taiwan. Electronic address:
Previous studies have shown that celecoxib or NSAID may paradoxically induce cyclooxygenase-2 (COX-2) expression and trigger inflammation-like responses in airway smooth muscle cells and renal mesangial cells. Despite the extensive research on celecoxib, its atypical biological effect on the induction of COX-2 in astroglial cells within the central nervous system (CNS) remains unexplored. In the present study, we investigated the impact of celecoxib on COX-2 and Glial Fibrillary Acidic Protein (GFAP) expression and explored the mechanisms underlying celecoxib-regulated COX-2 expression in cortical astrocytes of rats.
View Article and Find Full Text PDFCNS Neurosci Ther
December 2024
The Collaborative Innovation Center of Tissue Damage Repair and Regeneration Medicine of Zunyi Medical University, Zunyi, Guizhou, China.
Objective: The study investigates whether the expression and function of ENT1 can be regulated by inhibiting the JNK signaling pathway, thereby altering the levels of extracellular adenosine and glutamate in neurons, and subsequently affecting the progression of epilepsy.
Methods: The adult male SD rats were randomly divided into four groups: EP + SP600125 group, EP + DMSO group, EP group, and normal control group. The expression levels of ENT1, p-JNK, and JNK in the hippocampus of rats from each experimental group were detected using Western blotting technology.
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