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Anti-neuroinflammatory and Neuroprotective Effects of T-006 on Alzheimer's Disease Models by Modulating TLR4-Mediated MyD88/ NF-κB Signaling.
CNS Neurol Disord Drug Targets
January 2025
School of Medicine, Foshan University, Foshan, 528000, China.
Introduction: Neuroinflammation derived from the activation of the microglia is considered a vital pathogenic factor of Alzheimer's Disease (AD). T-006, a tetramethylpyrazine derivative, has been found to alleviate cognitive deficits via inhibiting tau expression and phosphorylation in AD transgenic mouse models. Recently, T-006 has been proven to dramatically decrease the levels of total Amyloid β (Aβ) peptide and Glial Fibrillary Acidic Protein (GFAP) and suppress the expression of ionized calcium binding adaptor molecule-1 (Iba-1) in APP/PS1 mice.
View Article and Find Full Text PDFG-protein-coupled estrogen receptor 30 regulation of signaling downstream of protein kinase Cε mediates sex dimorphism in hyaluronan-induced antihyperalgesia.
Pain
October 2024
Department of Oral and Maxillofacial Surgery, UCSF Pain and Addiction Research Center, University of California at San Francisco, San Francisco, California.
High molecular weight hyaluronan (HMWH) inhibits hyperalgesia induced by diverse pronociceptive inflammatory mediators and their second messengers, in rats of both sexes. However, the hyperalgesia induced by ligands at 3 pattern recognition receptors, lipopolysaccharide (a toll-like receptor 4 agonist), lipoteichoic acid (a toll-like receptor 2/6 agonist), and nigericin (a NOD-like receptor family, pyrin domain containing 3 activator), and oxaliplatin and paclitaxel chemotherapy-induced peripheral neuropathy are only attenuated in males. After gonadectomy or intrathecal administration of an antisense to G-protein-coupled estrogen receptor 30 (GPER) mRNA, HMWH produces antihyperalgesia in females.
View Article and Find Full Text PDFDeterminants of agricultural employment during the COVID-19 pandemic: A spatial analysis of Brazilian municipalities.
PLoS One
January 2025
School of Business, Pontifical Catholic University of Rio Grande do Sul (PUCRS), Porto Alegre, RS, Brazil.
The impact of COVID-19 has extended beyond the health toll it has taken on populations. The global economy has experienced significant downturns, with unemployment rates reaching unprecedented highs for this century. Nonetheless, the agricultural sector has been uniquely affected by the pandemic, particularly given its crucial role in food supply.
View Article and Find Full Text PDF[Protective effect of tumor necrosis factor receptor-associated factor 6 inhibitor C25-140 on acute kidney injury induced by diquat poisoning in mice].
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue
December 2024
Department of Emergency, Kweichow Moutai Hospital, Renhuai 564500, Guizhou, China. Corresponding author: Ou Renyang, Email:
Objective: To investigate the protective effect and mechanism of tumor necrosis factor receptor-associated factor 6 (TRAF6) inhibitor C25-140 on acute kidney injury (AKI) induced by acute diquat (DQ) poisoning in mice.
Methods: A total of 80 SPF grade healthy male C57BL/6 mice were randomly divided into the normal control group, DQ model group, C25-140 intervention group, and C25-140 control group, with 20 mice in each group. The DQ poisoning mouse model was established by using one-time intraperitoneal injection of 1 mL of 40 mg/kg DQ solution.
Staphylococcus aureus vesicles impair cutaneous wound healing through p38 MAPK-MerTK cleavage-mediated inhibition of macrophage efferocytosis.
Cell Commun Signal
January 2025
School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, 510515, China.
Background: Staphylococcus aureus, a known contributor to non-healing wounds, releases vesicles (SAVs) that influence the delicate balance of host-pathogen interactions. Efferocytosis, a process by which macrophages clear apoptotic cells, plays a key role in successful wound healing. However, the precise impact of SAVs on wound repair and efferocytosis remains unknown.
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