Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 180, P. 117513 - 117513
Published: Sept. 27, 2024
Language: Английский
Phytomedicine, Journal Year: 2024, Volume and Issue: 126, P. 155458 - 155458
Published: Feb. 22, 2024
Language: Английский
Citations
28
Frontiers in Pharmacology, Journal Year: 2022, Volume and Issue: 13
Published: Sept. 13, 2022
Cartilage endplate (CEP) plays important roles in the onset and progression of intervertebral disc degeneration (IVDD). Icariin (ICA) is major active ingredient Herba Epimedii has various biological activities such as anti-inflammatory antioxidant, which used to treat many degenerative diseases. However, effects mechanism ICA on chondrocytes are still unclear. Herein, we studied CEP elucidated underlying mechanisms. Endplate were isolated, TNF-α TBHP applied mimic an IVDD pathological environment. Also, mice model was established by transection bilateral facet joints investigate protective effect vivo. We found that treatment inhibited apoptosis decrease extracellular matrix production a dose-dependent manner. Our vivo experiments demonstrated could ameliorate development calcification. also ICA-activated Nrf-2/HO-1 pathway thus promoted Parkin-mediated mitophagy process ferroptosis, alleviated redox imbalance mitochondrial dysfunction eventually improved cell survival. Knockdown Nrf-2 using siRNA reversed degeneration. In conclusion, our study protect against calcification under conditions, associated may be related Nrf-2/HO-1-mediated activation ferroptosis inhibition. results suggest potential effective medicine for prevention treatment.
Language: Английский
Citations
40
Scientific Reports, Journal Year: 2023, Volume and Issue: 13(1)
Published: Sept. 1, 2023
Abstract Oxaliplatin is widely used in chemotherapy for colorectal cancer (CRC), but its sensitivity has become a major obstacle to limiting efficacy. Many literatures reported that Nrf2 activation promoted tumor chemoresistance. In this study, we explored the role and mechanism of inhibition oxaliplatin-based chemosensitivity CRC. vitro experiments, applied 4-octyl itaconate (4-OI) activate Nrf2, lentivirus knock down CRC cell lines. By measuring viability, colony formation, apoptosis, reactive oxygen species production, western blot, found oxaliplatin lobaplatin suppressed growth HCT-116 LOVO cells dose-dependent manner, expression Nrf2. 4-OI, an activator, reduced sensibility lobaplatin, while knockdown lobaplatin. Through public databases, GPX4 normal tissues was lower compared with CRC, high predicted poor prognosis. Meanwhile, vitro. The enhanced effects reduce GSH content, increase MDA which oxaliplatin-induced ferroptosis. Subsequently, GSDME-N, induced LDH, IL-1β, TNF-a release, aggravated occurrence GSMDE-mediated pyroptosis. Finally, on HCT116 xenograft vivo. Thus, our study showed improved by promoting ferroptosis pyroptosis, provided new target overcoming chemoresistance
Language: Английский
Citations
32
Bioactive Materials, Journal Year: 2024, Volume and Issue: 38, P. 438 - 454
Published: May 12, 2024
Spinal cord injury (SCI) is a traumatic condition that results in impaired motor and sensory function. Ferroptosis one of the main causes neural cell death loss neurological function spinal cord, ferroptosis inhibitors are effective reducing inflammation repairing SCI. Although human umbilical mesenchymal stem cells (Huc-MSCs) can ameliorate inflammatory microenvironments promote regeneration SCI, their efficacy greatly limited by local microenvironment after Therefore, this study, we constructed drug-release nanoparticle system with synergistic Huc-MSCs inhibitor, which anchored Tz-A6 peptide based on CD44-targeting sequence, combined reactive oxygen species (ROS)-responsive drug nanocarrier mPEG-b-Lys-BECI-TCO at other end for SCI repair. Meanwhile, also modified classic inhibitor Ferrostatin-1 (Fer-1) synthesized new prodrug Feborastatin-1 (Feb-1). The showed treatment regimen significantly inhibited response promoted recovery rats This study developed combination therapy provides strategy construction drug-coordinated system.
Language: Английский
Citations
13
Gastroenterology, Journal Year: 2024, Volume and Issue: 167(2), P. 231 - 249
Published: March 1, 2024
Language: Английский
Citations
11
Oxidative Medicine and Cellular Longevity, Journal Year: 2022, Volume and Issue: 2022, P. 1 - 12
Published: Oct. 12, 2022
Ferroptosis is a type of programmed cell death characterized by iron overload, oxidative stress, imbalance in lipid repair, and mitochondria-specific pathological manifestations. Growing number molecular mechanisms signaling pathways have been found to be involved ferroptosis progression, including metabolism, amino acid energy metabolism. It worth noting that the progression fibrotic diseases such as liver cirrhosis, cardiomyopathy, idiopathic pulmonary fibrosis, inhibition has acquired beneficial outcomes rodent models, while studies on renal fibrosis remains limited. Recent revealed targeting can effectively mitigate chronic kidney injury fibrosis. Moreover, myofibroblasts suffer from during fiber extracellular matrix deposition cascade reaction pharmacological modulation shows great therapeutic effect Here, we summarize latest high-quality review its potential
Language: Английский
Citations
29
Frontiers in Pharmacology, Journal Year: 2023, Volume and Issue: 14
Published: May 5, 2023
Ferroptosis is a new iron-dependent cell death mode, which different from the other types of programmed death, such as apoptosis, necrosis, and autophagy. characterized by process in fatal lipids lipid peroxidation accumulate cells eventually lead to death. Alcohol-related liver disease (ALD) type injury caused excessive alcohol intake. broad-spectrum category, includes fatty liver, steatohepatitis, hepatitis, cirrhosis, hepatocellular tumors. Recent studies have found that ferroptosis involved pathological development non-viral diseases. Therefore, may be an ideal target for treatment In this review article, we will elaborate molecular mechanism regulatory ferroptosis, explore key role process, summarize existing targeted drugs their feasibility disease.
Language: Английский
Citations
15
Chemico-Biological Interactions, Journal Year: 2023, Volume and Issue: 378, P. 110479 - 110479
Published: April 23, 2023
Language: Английский
Citations
14
Current Medicinal Chemistry, Journal Year: 2024, Volume and Issue: 31(19), P. 2821 - 2837
Published: Feb. 14, 2024
Introduction: Senescence of activated hepatic stellate cells (HSC) reduces extracellular matrix expression to reverse liver fibrosis. Ferroptosis is closely related cellular senescence, but its regulatory mechanisms need be further investigated. The iron ions weakly bound ferritin in the cell are called labile pool (LIP), and together with ferritin, they maintain homeostasis regulate cell's sensitivity ferroptosis. Methods: We used lipopolysaccharide (LPS) construct a pathological model group divided into blank group, curcumol 12.5 mg/L 25 50 group. HIF-1α-NCOA4- FTH1 signalling axis, ferroptosis senescence were detected by various molecular biology experiments. Result: found that could induce promoting death cells. Curcumol induced massive deposition activating HIF-1α-NCOA4-FTH1 which led overload lipid peroxidation-induced Interestingly, our knockdown HIF-1α rescued curcumol-induced LIP cells, suggesting key target regulating metabolism able rescue when we reduced ion using chelators. Conclusion: Overall, induces increasing NCOA4 interaction FTH1, leading ions, may biological mechanism anti-liver
Language: Английский
Citations
5
Chemical Engineering Journal, Journal Year: 2024, Volume and Issue: 495, P. 153592 - 153592
Published: June 28, 2024
Language: Английский
Citations
5