Mechanistic Insights into T-2 Toxin-Induced Thymic Epithelial Cell Injury and Immunotoxicity via the ROS-NF-κB-NLRP3 Signaling Axis DOI
Yanfang Zhang, Mingyan Chen, Ruiyan Niu

и другие.

Journal of Agricultural and Food Chemistry, Год журнала: 2025, Номер unknown

Опубликована: Май 19, 2025

Thymic epithelial cells (TECs) are critical for thymic structure and function, yet the impact of T-2 toxin (T-2) on TECs related molecular pathways remains unclear. This study sheds light mechanisms T-2-induced TEC damage, focusing ROS-NF-κB-NLRP3 signaling axis. The in vivo vitro analyses suggest that induces injury through ROS-driven NLRP3 inflammasome activation, NF-κB signaling, inflammation, apoptosis. Molecular docking analysis verified binding to components involved oxidative stress, inflammatory pathways, These findings were further supported by therapeutic interventions targeting ROS NLRP3. N-acetylcysteine (NAC) effectively reduced levels, suppressed inhibited mitigated inflammation apoptosis, effects mirrored inhibitor MCC950, emphasizing role ROS-mediated activation damage. Concurrently, inhibition apoptosis MTEC1 cells, pivotal function axis pathogenesis injury. Our offers an in-depth insight into driving immunotoxicity identifies potential strategies these mitigate preserve immune function.

Язык: Английский

Inhibition of N6-methyladenosine methylation of ASC by berberine ameliorates pyroptosis of renal tubular epithelial cells in acute kidney injury DOI Creative Commons
Jiacheng Li, Linxiao Lv, Mingyang Hu

и другие.

Cellular Signalling, Год журнала: 2025, Номер unknown, С. 111732 - 111732

Опубликована: Март 1, 2025

Acute kidney injury (AKI) lacks a definitive therapeutic approach beyond supportive care. One significant pathological mechanism involves the regulated death of tubular epithelial cells; however, regulatory mechanisms underlying this cell pathway require further investigation. The N6-methyladenosine (m6A) modification, recognized as most prevalent modification in eukaryotes, plays critical role processes associated with AKI. Here, study investigates association between methyltransferase-like 3 (METTL3) and pyroptosis mice folic acid (FA)-induced Both vitro vivo experiments have confirmed that METTL3 AKI progression, correlating renal inflammation. Moreover, RNA immunoprecipitation quantitative PCR (RIP-qPCR) analysis demonstrated METTL3-mediated m6A methylation occurred mRNA Apoptosis-associated speck-like protein containing CARD (ASC) H2O2-induced (TCMK-1) cells. Notably, knockdown resulted reduced ASC expression, decreased release inflammatory factors, pyroptosis. In addition, we verified inhibitory effect berberine hydrochloride, monomer used traditional Chinese medicine, on expression. We also ameliorated FA-induced TCMK-1 cells by inhibiting modulating ASC/caspase-1/Gasdermin D axis. These findings provide insights into targeted therapies drug development for

Язык: Английский

Процитировано

0
Mechanistic Insights into T-2 Toxin-Induced Thymic Epithelial Cell Injury and Immunotoxicity via the ROS-NF-κB-NLRP3 Signaling Axis DOI
Yanfang Zhang, Mingyan Chen, Ruiyan Niu

и другие.

Journal of Agricultural and Food Chemistry, Год журнала: 2025, Номер unknown

Опубликована: Май 19, 2025

Thymic epithelial cells (TECs) are critical for thymic structure and function, yet the impact of T-2 toxin (T-2) on TECs related molecular pathways remains unclear. This study sheds light mechanisms T-2-induced TEC damage, focusing ROS-NF-κB-NLRP3 signaling axis. The in vivo vitro analyses suggest that induces injury through ROS-driven NLRP3 inflammasome activation, NF-κB signaling, inflammation, apoptosis. Molecular docking analysis verified binding to components involved oxidative stress, inflammatory pathways, These findings were further supported by therapeutic interventions targeting ROS NLRP3. N-acetylcysteine (NAC) effectively reduced levels, suppressed inhibited mitigated inflammation apoptosis, effects mirrored inhibitor MCC950, emphasizing role ROS-mediated activation damage. Concurrently, inhibition apoptosis MTEC1 cells, pivotal function axis pathogenesis injury. Our offers an in-depth insight into driving immunotoxicity identifies potential strategies these mitigate preserve immune function.

Язык: Английский

Процитировано

0