This study was conducted to examine the effects and mechanisms of hypoxia-preconditioned human dental pulp stem cells (H-hDPSCs) transplantation on microglial pyroptosis in neonatal rats with hypoxic-ischemic brain damage (HIBD). The hDPSCs were extracted using the tissue block method and identified by immunofluorescence staining. The HIBD model was constructed using the classical Rice-Vannucci method. 24 h after HIBD, normoxic preconditioning hDPSCs (N-hDPSCs) and H-hDPSCs were transplanted into the lateral ventricle. The brain damage was examined by hematoxylin & eosin and Nissl stainings 72 h after transplantation. The expression of signal transducer and activator of transcription 3 (STAT3)/NOD-like receptor family pyrin domain-containing 3 (NLRP3)/Caspase-1 axis-related proteins was analyzed by immunofluorescence staining and western blots. Tissue levels of interleukin-1 beta (IL-1β) were derived from ELISA. After modeling, the neural cells in the HIBD group were disordered and sparsely scattered, with a deficiency of nitrosamines. The data revealed that the phosphorylated STAT3, NLRP3, Cleaved-Caspase 1, N-terminal fragment of gasdermin D (GSDMD-N), and IL-1β protein expression were significantly lower in the H-hDPSCs and N-hDPSCs groups compared to the HIBD group. The protein expression in the H-hDPSCs group was considerably lower than in the N-hDPSCs group. H-hDPSCs may protect microglia from pyroptosis by regulating the STAT3/NLRP3/Caspase-1/GSDMD axis to alleviate inflammatory damage, and attenuate HIBD in newborn rats at the same time. Moreover, the therapeutic effect of H-hDPSCs transplantation was superior to that of N-hDPSCs transplantation.
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http://dx.doi.org/10.1097/WNR.0000000000002144 | DOI Listing |
Cells
February 2025
Institute of Molecular Medicine, National Tsing Hua University, No. 101, Section 2, Kuang-Fu Road, Hsinchu 300044, Taiwan.
Brain injuries can result from accidents, warfare, sports injuries, or brain diseases. Identifying regeneration-associated genes (RAGs) during epigenome remodeling upon brain injury could have a significant impact on reducing neuronal death and subsequent neurodegeneration for patients with brain injury. We previously identified several WNT genes as RAGs involved in the neurite regrowth of injured cortical neurons.
View Article and Find Full Text PDFBackground: Acquired brain injury (ABI), including traumatic brain injury and hypoxic/anoxic injury, presents significant public health concerns; however, existing literature has focused primarily on male populations, such as military personnel and contact sports participants. Sex-related differences in ABI outcomes necessitate focused research due to potential heightened risk and distinct physiological responses among females.
Objectives: This pilot study aims to explore fluid-based biomarkers for neurological injury and inflammation in females experiencing intimate partner violence (IPV)-related assaults to the head, neck, or face.
AJR Am J Roentgenol
March 2025
Marcus Institute for Brain Health and Departments of Radiology and Neurology, University of Colorado School of Medicine, 12631 East 17th Place, Aurora, CO 80045.
Brain
March 2025
School of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China.
Patients with anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis, often present with severe psychiatric symptoms, yet the neuropathological mechanisms underlying their cognitive deficits remain insufficiently understood. In this study, we constructed an animal model using anti-NMDAR IgG purified from the serum of patients with anti-NMDAR encephalitis, and we used IgG obtained from healthy individuals as a control. Daily administration of anti-NMDAR IgG into the medial prefrontal cortex (mPFC) of mice for 7 days resulted in cognitive impairments resembling clinical symptoms, which spontaneously resolved 30 days after discontinuing the injections.
View Article and Find Full Text PDFFront Aging Neurosci
February 2025
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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