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Suppression of Sepsis Cytokine Storm by Escherichia Coli Cell Wall-Derived Carbon Dots.
Adv Mater
January 2025
State Key Laboratory of Medicinal Chemical Biology and College of Pharmacy, Nankai University, Tianjin, 300350, China.
Article Synopsis
- Sepsis is a severe condition caused by an uncontrolled immune reaction to infections, often involving harmful bacteria like E. coli, and currently lacks effective treatments.
- Researchers developed E. coli wall-derived carbon dots (E-CDs) that can reduce inflammation and improve survival rates in septic mice by binding to immune receptors and preventing excessive immune responses.
- E-CDs also show promise in other models, reducing inflammation and oxidative stress, suggesting they could be a new therapeutic approach for treating sepsis by utilizing pathogen-derived materials.
Elevated IL-6 Expression in Autologous Adipose-Derived Stem Cells Regulates RANKL Mediated Inflammation in Osteoarthritis.
Cells
December 2024
Orthopedic Surgery, Inha University Hospital, Incheon 22332, Republic of Korea.
Interleukin-6 (IL-6) expression in mesenchymal stem cells (MSCs) has been shown to play a pivotal role in modulating cartilage regeneration and immune responses, particularly in the context of diseases that involve both degenerative processes and inflammation, such as osteoarthritis (OA). However, the precise mechanism through which IL-6 and other immune-regulatory factors influence the therapeutic efficacy of autologous adipose-derived stem cells (ASCs) transplantation in OA treatment remains to be fully elucidated. This study aims to investigate the relationship between IL-6 expression in autologous ASCs isolated from OA patients and their impact on immune modulation, particularly focusing on the regulation of Receptor Activator of Nuclear factor Kappa-Β Ligand (RANKL), a key mediator of immune-driven cartilage degradation in OA.
View Article and Find Full Text PDFIdentification of Marine Compounds Inhibiting NF-κBInducing Kinase Through Molecular Docking and Molecular Dynamics Simulations.
Biomolecules
November 2024
Department of Pharmacology, Kangwon National University School of Medicine, Chuncheon 24341, Republic of Korea.
NF-κB-inducing kinase (NIK) plays a pivotal role in regulating both the canonical and non-canonical NF-κB signaling pathways, driving the expression of proteins involved in inflammation, immune responses, and cell survival. Overactivation of NIK is linked to various pathological conditions, including chronic inflammation, autoimmune diseases, metabolic disorders, and cancer progression. As such, NIK represents a compelling target for therapeutic intervention in these diseases.
View Article and Find Full Text PDFPuerarin pretreatment provides protection against myocardial ischemia/reperfusion injury via inhibiting excessive autophagy and apoptosis by modulation of HES1.
Sci Rep
January 2025
Department of Cardiovascular Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwai Road, Nanchang, 330006, Jiangxi, China.
The study aimed to elucidate the underlying pharmacological mechanism of the traditional Chinese medicine Pue in ameliorating myocardial ischemia-reperfusion injury (MIRI), a critical clinical challenge exacerbated by reperfusion therapy. In vivo MIRI and in vitro anoxia/reoxygenation (A/R) models were constructed. The results demonstrated that Pue pretreatment effectively alleviated MIRI, as manifested by diminishing the levels of serum CK-MB and LDH, mitigating the extent of myocardial infarction and enhancing cardiac functionality.
View Article and Find Full Text PDFInhibition of PGAM5 hyperactivation reduces neuronal apoptosis in PC12 cells and experimental vascular dementia rats.
Arch Gerontol Geriatr
December 2024
Neurology Ward 1, The First Affiliated Hospital of Guangxi University of Chinese Medicine, Qingxiu District, Nanning, 530001, China. Electronic address:
Purpose: The incidence of vascular dementia (VaD), as one of the main types of dementia in old age, has been increasing year by year, and exploring its pathogenesis and seeking practical and effective treatment methods are undoubtedly the key to solving this problem. Phosphoglycerate translocase 5 (PGAM5), as a crossroads of multiple signaling pathways, can lead to mitochondrial fission, which in turn triggers the onset and development of necroptosis, and thus PGAM5 may be a novel target for the prevention and treatment of vascular dementia.
Methods: Animal model of vascular dementia was established by Two-vessel occlusion (2-VO) method, and cellular model of vascular dementia was established by oxygen glucose deprivation (OGD) method.
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