circHOMER1 Alleviates Sevoflurane‐Induced Hippocampal Neuronal Injury via Targeted Negative Regulation of miR‐217

Journal of Biochemical and Molecular Toxicology, Journal Year: 2025, Volume and Issue: 39(1)

Published: Jan. 1, 2025

ABSTRACT Sevoflurane (Sev) is a widely applied anesthetic in clinical practice; however, it could induce neurotoxicity and lead to postoperative cognitive dysfunction (POCD). This study aimed investigate the role underlying mechanism of circHOMER1 Sev‐induced POCD. Sev treated mouse hippocampal neuronal HT22 cells SD rats. RT‐qPCR was used detect levels miR‐217. ELISA employed measure inflammatory factors IL‐6, IL‐1β, TNF‐α. Commercially available kits assessed concentration MDA measured activities LDH SOD. The CCK‐8 assay cell viability. Flow cytometry analyzed apoptosis. Morris water maze test evaluated learning abilities Dual luciferase reporter assays RIP experiments validated targeted binding treatment significantly reduces viability, increases apoptosis, stimulates responses oxidative stress, induces memory impairments Following exposure Sev, expression markedly decreased, while overexpression can alleviate neuroinflammation, deficits CircHOMER1 targets miR‐217, transfection miR‐217 antagonizes neuroprotective effects circHOMER1. demonstrated that negatively regulated thereby inhibiting disorders.

Language: Английский

CD36 Induces Inflammation by Promoting Ferroptosis in Pancreas, Epididymal Adipose Tissue, and Adipose Tissue Macrophages in Obesity-Related Severe Acute Pancreatitis

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(8), P. 3482 - 3482

Published: April 8, 2025

Severe acute pancreatitis (SAP) is mainly triggered by the abnormal activation of pancreatic enzymes. Obesity acts as an independent risk factor for SAP; however, underlying mechanism has not been fully elucidated. In this study, SAP models were established in mice with normal and high-fat diets. Subsequently, study examined ferroptosis inflammatory markers pancreas epididymal adipose tissues. To mimic obesity-related tissue macrophages (ATMs), lipopolysaccharide (LPS) palmitic acid (PA) introduced, alterations inflammation assessed. elucidate regulatory role cluster differentiation 36 (CD36) ferroptosis, liproxstatin-1 (Lip-1) sulfosuccinimidyl oleate sodium (SSO) utilized in-depth analysis pancreas, tissues, ATMs. Our findings suggest that obesity aggravates tissue, ATMs during SAP, evidenced increased lipid peroxidation, elevated Fe2+ levels, markers, while these regained Lip-1. Notably, CD36 levels significantly ATMs, indicating promotes induces inflammation. SSO treatment alleviated changes reduced Western blot results showed promoted through acyl-CoA synthetase long-chain family member 4 (ACSL4)/glutathione peroxidase (GPX4) axis a similar was mediated ferritin heavy chain 1 (FTH1)/GPX4 These demonstrate facilitating SAP. The inhibition could provide novel viewpoints prevention

Language: Английский