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Identification of anti-SARS-CoV-2 compounds from Qingwen Zhike prescription and exploration of their underlying mechanism by UPLC-Q-Exactive Orbitrap MS, high-throughput screening assays and transmission electron microscopy.
J Pharm Biomed Anal
December 2024
Beijing Research Institute of Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China. Electronic address:
Qingwen Zhike prescription (QWZK), a traditional Chinese medicine (TCM) hospital prescription developed in response to the corona virus disease 2019 (COVID-19) pandemic, has demonstrated efficacy in clinical practice. Nevertheless, its specific antiviral components and mechanisms of action remain unclear. This study screened the antiviral compounds against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) from Qingwen Zhike prescription and explored the underlying mechanism through chemical composition analysis, serum and lung exposure profiles analysis, high-throughput screening, and transmission electron microscopy (TEM) observation.
View Article and Find Full Text PDFAntiviral activity of an ACE2-Fc fusion protein against SARS-CoV-2 and its variants.
PLoS One
January 2025
Immunology and Immunotherapy Division, Center of Molecular Immunology (CIM), Havana, Cuba.
SARS-CoV-2 has continued spreading around the world in recent years since the initial outbreak in 2019, frequently developing into new variants with greater human infectious capacity. SARS-CoV-2 and its mutants use the angiotensin-converting enzyme 2 (ACE2) as a cellular entry receptor, which has triggered several therapeutic strategies against COVID-19 relying on the use of ACE2 recombinant proteins as decoy receptors. In this work, we propose an ACE2 silent Fc fusion protein (ACE2-hFcLALA) as a candidate therapy against COVID-19.
View Article and Find Full Text PDFIL-6 Promotes Muscle Atrophy by Increasing Ubiquitin-Proteasome Degradation of Muscle Regeneration Factors After Cerebral Infarction in Rats.
Neuromolecular Med
January 2025
Department of Rehabilitation Medicine, The Affiliated Jiangning Hospital of Nanjing Medical University, No. 168 Gushan Road, Dongshan Street, Jiangning District, Nanjing, 211199, Jiangsu, China.
Muscle atrophy in pathological or diseased muscles arises from an imbalance between protein synthesis and degradation. Elevated levels of interleukin-6 (IL-6) are a hallmark of ischemic stroke and have been associated with muscle atrophy in certain pathological contexts. However, the mechanisms by which IL-6 induces muscle atrophy in the context of stroke remain unclear.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Background: The proteasome plays key roles in synaptic plasticity and memory by regulating protein turnover, quality control, and elimination of oxidized/misfolded proteins. Here, we investigate proteasome function and localization at synapses in Alzheimer's disease (AD) post-mortem brain tissue and in experimental models.
Method: We used primary hippocampal cultures, amyloid-β oligomers (AβO)-injected or transgenic animal models, and human brain tissue to determine brain proteasome function and subcellular localization.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Icahn School of Medicine at Mount Sinai Medical Center, New York, NY, USA.
Background: Presenilin1 (PS1)/γ-secretase cleaves within the transmembrane domain of numerous receptor substrates. Mutations in PS1 have implications on the catalytic subunit of γ-secretase decreasing its activity and becoming a potential causative factor for Familial Alzheimer's Disease (FAD). This work studies the role of PS1/γ-secretase on the processing, angiogenic signaling, and functions of VEGFR2 and the effects of PS1 FAD mutants on the γ-secretase-mediated epsilon cleavage of VEGFR2.
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