Nano Research, Journal Year: 2024, Volume and Issue: 18(2), P. 94907175 - 94907175
Published: Dec. 16, 2024
Language: Английский
Biomaterials Advances, Journal Year: 2025, Volume and Issue: 169, P. 214193 - 214193
Published: Jan. 18, 2025
Language: Английский
Citations
2
Chemical Engineering Journal, Journal Year: 2025, Volume and Issue: unknown, P. 160592 - 160592
Published: Feb. 1, 2025
Language: Английский
Citations
1
Advanced Healthcare Materials, Journal Year: 2024, Volume and Issue: 13(22)
Published: April 22, 2024
Chronic local inflammation and excessive cell apoptosis in nucleus pulposus (NP) tissue are the main causes of intervertebral disc degeneration (IDD). Stimuli-responsive hydrogels have great potential treatment IDD by facilitating localized controlled drug delivery. Herein, an injectable drug-loaded dual stimuli-responsive adhesive hydrogel for microenvironmental regulation IDD, is developed. The gelatin methacryloyl functionalized with phenylboronic acid groups to enhance loading capacity enable behavior, while incorporation oxidized hyaluronic further improves properties. prepared exhibits enhanced diol-containing drugs, pH- reactive oxygen species (ROS)-responsive behaviors, excellent radical scavenging efficiency, potent antibacterial activity, favorable biocompatibility. Furthermore, shows a beneficial protective efficacy on NP cells within vitro oxidative stress microenvironment. vivo results demonstrate hydrogel's therapeutic effect treating maintaining water retention, restoring height, promoting regeneration, indicating that this holds as promising approach regulating microenvironment alleviating progression IDD.
Language: Английский
Citations
7
Cell Biology and Toxicology, Journal Year: 2024, Volume and Issue: 40(1)
Published: March 13, 2024
Abstract Intervertebral disc degeneration (IVDD) is an aging disease that results in a low quality of life and heavy socioeconomic burden. The mitochondrial unfolded protein response (UPR mt ) take part various aging-related diseases. Our research intents to explore the role underlying mechanism UPR IVDD. Nucleus pulposus (NP) cells were exposed IL-1β nicotinamide riboside (NR) served as inducer treat NP cells. Detection ATP, NAD + NADH used determine function mitochondria. MRI, Safranin O-fast green Immunohistochemical examination degree IVDD vivo. In this study, we discovered was increased markedly human tissues than healthy controls. vitro, mitophagy levels promoted treated with IL-1β. Upregulation by NR Atf5 overexpression inhibited cell apoptosis further improved mitophagy. Silencing Pink1 reversed protective effects induced . vivo, might attenuate IDD activating rats. summary, involved regulating Pink1-induced Mitophagy be latent target for Graphical • upregulated degenerative intervertebral disc. regulated could activate protect from apoptosis. Nicotinamide reduced apoptosis, thereby delaying process
Language: Английский
Citations
6
Advanced Healthcare Materials, Journal Year: 2024, Volume and Issue: 13(29)
Published: July 22, 2024
Reactive oxygen species (ROS), as metabolic byproducts, play pivotal role in physiological and pathological processes. Recently, studies on the regulation of ROS levels for disease treatments have attracted extensive attention, mainly involving ROS-induced toxicity therapy mediated by producers antioxidant scavengers. Nanotechnology advancements led to development numerous nanomaterials with ROS-modulating capabilities, among which carbon dots (CDs) standing out noteworthy nanomedicines own their distinctive physicochemical properties, high stability, excellent biocompatibility. Despite progress treating ROS-related diseases based CDs, critical issues such rational design principles remain underexplored. The primary cause these may stem from intricate amalgamation core structure, defects, surface states, inherent poses challenges establishing a consistent generalization. This review succinctly summarizes recently ROS-modulated approaches using CDs treatment. Specifically, it investigates established therapeutic strategies CDs-regulated ROS, emphasizing interplay between intrinsic structure generation or scavenging ability. conclusion raises several unresolved key scientific prominent technological bottlenecks, explores future perspectives comprehensive CDs-based therapy.
Language: Английский
Citations
6
Chemical Engineering Journal, Journal Year: 2024, Volume and Issue: 498, P. 155389 - 155389
Published: Aug. 31, 2024
Language: Английский
Citations
5
Acta Biomaterialia, Journal Year: 2024, Volume and Issue: 186, P. 1 - 29
Published: Aug. 14, 2024
Language: Английский
Citations
4
International Journal of Biological Macromolecules, Journal Year: 2025, Volume and Issue: 295, P. 139535 - 139535
Published: Jan. 5, 2025
Language: Английский
Citations
0
Journal of Investigative Surgery, Journal Year: 2025, Volume and Issue: 38(1)
Published: Feb. 2, 2025
The incidence of lumbar disk herniation (LDH) is usually caused by degeneration. Surgery a common treatment strategy for LDH, but it can recur, resulting in recurrent (RDH). To explore the predictive value hsa-miR-4741 and LILRB2 prognosis LDH surgery mechanism nucleus pulposus senescence. ROC curves RDH based on were constructed to evaluate their values surgery. Human cells (NPC) was treated TNF-α construct cell senescence model, studying mechanism. Oxidative stress markers detected after overexpression effects NPC. Dual luciferase assay transfection mimics or inhibitor used investigate targeted regulation LILRB2. combination showed higher accuracy predicting outcome (AUC = 0.9367), compared with single molecule. Overexpression enhanced TNF-α-induced oxidative senescence, while had opposite effect. Hsa-miR-4741 attenuated activity NPC transfected wt-LILRB2 vector significantly down-regulated expression. In addition, antioxidant NAC reversed promotion good predictor prognosis. promoted stress-induced negatively regulating
Language: Английский
Citations
0
Dyes and Pigments, Journal Year: 2025, Volume and Issue: unknown, P. 112718 - 112718
Published: Feb. 1, 2025
Language: Английский
Citations
0