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Kaempferol has been reported to act as an anti-inflammatory agent in LPS-induced neuroinflammation in vitro and in vivo, but its role in the inflammation after cerebral ischemia/reperfusion (I/R) is unclear. The present study was to investigate the effect of kaempferol on inflammation in ischemic brain tissue and explore its mechanisms in cerebral I/R rats. Cerebral I/R rat model was established by middle cerebral artery occlusion for 60 min and following reperfusion. Kaempferol at doses of 25, 50 and 100 mg/kg was administered for 7 days after cerebral I/R. Kaempferol treatment significantly reduced cerebral infarct volume, attenuated inflammation and blood-brain barrier (BBB) disruption after cerebral I/R, thus improved neurological outcomes at the day 7 after cerebral I/R. Furthermore, the results also showed kaempferol treatment decreased the phosphorylation and nuclear transposition of transcription factor NF-κB p65, thus inhibited expression of various pro-inflammatory proteins. In conclusion, kaempferol attenuates neuroinflammation and blood brain barrier dysfunction to improve neurological deficits in cerebral I/R rats, its mechanism is related to NF-κB pathway.
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http://dx.doi.org/10.1016/j.brainres.2019.146361 | DOI Listing |
Compr Physiol
October 2025
School of Pharmacy and Medical Sciences, Griffith University, Southport, Queensland, Australia.
Mechanisms underlying cardiovascular, affective, and metabolic (CAM) multimorbidity are incompletely defined. We assessed how two risk factors-chronic stress (CS) and a Western diet (WD)-interact to influence cardiovascular function, resilience, adaptability, and allostatic load (AL); explore pathway involvement; and examine relationships with behavioral, metabolic, and systemic AL. Male C57Bl/6 mice (8 weeks old, n = 64) consumed a control (CD) or WD (12%-65%-23% or 32%-57%-11% calories from fat-carbohydrate-protein) for 17 weeks, with half subjected to 2 h daily restraint stress over the final 2 weeks (CD + CS and WD + CS).
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 PDFNeuroscience
September 2025
Research Group "Synapto-Oscillopathies", Institute of Biology, Otto-von-Guericke-University, Magdeburg, Germany; Department of Genetics and Molecular Neurobiology, Institute of Biology, Otto-von-Guericke University, Magdeburg, Germany; Center for Behavioral Brain Sciences (CBBS), Magdeburg, Germany.
Stress activates the hypothalamic-pituitary-adrenal (HPA) axis, releasing corticosterone (CORT), which binds to glucocorticoid (GR) and mineralocorticoid (MR) receptors in the brain. While stress influences behaviorally relevant network oscillations in limbic regions such as the hippocampus, amygdala, and prefrontal cortex, the direct effects of CORT on these oscillations remain unclear. We examined the acute impact of CORT on anterior cingulate cortex (ACC) oscillations in adult male mice, a hub region for stress and anxiety regulation.
View Article and Find Full Text PDFActa Pharm Sin B
August 2025
Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan 250012, China.
Receptor-interacting protein kinase 1 (RIPK1) plays an essential role in regulating the necroptosis and apoptosis in cerebral ischemia-reperfusion (I/R) injury. However, the regulation of RIPK1 kinase activity after cerebral I/R injury remains largely unknown. In this study, we found the downregulation of protein arginine methyltransferase 1 (PRMT1) was induced by cerebral I/R injury, which negatively correlated with the activation of RIPK1.
View Article and Find Full Text PDFSignal Transduct Target Ther
September 2025
Division of Cardiology and Angiology, University Hospital Magdeburg, Magdeburg, Germany.
Cardiovascular diseases are the leading cause of morbidity and mortality worldwide. The central underlying mechanisms of cardiovascular diseases are vascular aging and associated arterial stiffness. Arterial stiffness is characterized by structural (e.
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