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p38γ modulates ferroptosis in brain injury caused by ethanol and cerebral ischemia/reperfusion by regulating the p53/SLC7A11 signaling pathway.
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Department of Neurology, Northwest University School of Medicine, Xi'an 710068, China; Northwest University First Hospital, Xi'an 710043, China. Electronic address:
Ischemic stroke, a neurological condition with a complicated etiology that is accompanied by severe inflammation and oxidative stress, and ethanol (EtOH) may aggravate ischemia/reperfusion (I/R)-induced brain damage. However, the effect of prolonged alcohol intake on acute brain injury remains ambiguous. As part of the mitogen-activated protein kinase (MAPK) family, p38γ is involved in ferroptosis and inflammation in various diseases.
View Article and Find Full Text PDFRole of mitogen-activated protein kinase inhibitors in Alzheimer's disease: Rouge of brain kinases.
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Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour 22511, AlBeheira, Egypt. Electronic address:
Alzheimer's disease (AD) is the chief cause of dementia and related mortality worldwide due to progressive accumulation of amyloid peptide (Aβ) and hyperphosphorylated tau protein. These neuropathological changes lead to cognitive impairment and memory dysfunction. Notably, most Food drug Administration (FDA) approved anti-AD medications such as tacrine and donepezil are engaged with symptomatic relief of cognitive impairment but do not reverse the underlying AD neuropathology.
View Article and Find Full Text PDFInterdisciplinary integration strategy reveals the anti-inflammatory efficacy and potential mechanism of Jianpi Qingre Tongluo prescription in rheumatoid arthritis.
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Department of Rheumatology, The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui, 230031, China; First Clinical Medical School, Anhui University of Chinese Medicine, Hefei, Anhui, 230038, China.
Background: Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic synovitis and associated with high rates of disability and systemic damage. Jianpi Qingre Tongluo prescription (Huangqin Qingre Chubi Capsule, HQC), an herbal formula with abundant clinical applications, has played a definite role in both clinical and experimental studies of RA. However, the specific mechanisms by which HQC relieves inflammation in RA have not been fully elucidated.
View Article and Find Full Text PDFLysine-Proline-Valine peptide mitigates fine dust-induced keratinocyte apoptosis and inflammation by regulating oxidative stress and modulating the MAPK/NF-κB pathway.
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Major of Human Bio-convergence, Division of Smart Healthcare, Pukyong National University, Busan 48513, Republic of Korea. Electronic address:
Airborne particulate matter (PM) poses a major environmental risk that impairs skin health by triggering oxidative stress, inflammation, and cell death. In this study, we investigated the protective effects of Lysine-Proline-Valine (KPV)-an endogenous peptide derived from α-melanocyte-stimulating hormone-against oxidative damage and inflammation induced by fine PM (PM) in human HaCaT keratinocytes. Our results show that PM markedly suppresses HaCaT cell proliferation via cytotoxic effects and induces a pro-inflammatory response by increasing IL-1β secretion.
View Article and Find Full Text PDFThe role of protein phosphorylation modifications mediated by iron metabolism regulatory networks in the pathogenesis of Alzheimer's disease.
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Hospital of Encephalopathy, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
Alzheimer's disease (AD) is a severe neurodegenerative disease characterized mainly by the formation of amyloid beta (Aβ) plaques and abnormal phosphorylation of tau. In recent years, an imbalance in iron homeostasis has been recognized to play a key role in the pathological process of AD. Abnormal iron accumulation can activate various kinases such as glycogen synthase kinase-3β, cyclin-dependent kinase 5, and mitogen-activated protein kinase, leading to abnormal phosphorylation of tau and amyloid precursor protein, and accelerating the formation of Aβ plaques and neurofibrillary tangles.
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