Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)
Published: Oct. 26, 2024
Language: Английский
Molecular Medicine Reports, Journal Year: 2025, Volume and Issue: 31(3)
Published: Jan. 13, 2025
Calycosin‑7‑O‑β‑D‑glucoside (CG), a major active ingredient of Astragali Radix, exerts neuroprotective effects against cerebral ischemia; however, whether the CG are associated with mitochondrial protection remains unclear. The present study explored role in improving function HT22 cell model oxygen‑glucose deprivation/reperfusion (OGD/R). Cell Counting Kit‑8 assay, flow cytometry, immunofluorescence and western blotting were performed to investigate on function. results demonstrated that was restored after treatment CG, as indicated by reduced reactive oxygen species levels, increased membrane potential improved morphology. Overactivated mitophagy revealed be inhibited regulation proteins involved fission [phosphorylated‑dynamin‑related protein 1 (Drp1) Drp1] (LC3, p62 translocase outer 20), biogenesis enhanced levels sirtuin (SIRT1) peroxisome proliferator‑activated receptor γ coactivator‑1α (PGC‑1α). In addition, neuronal apoptosis ameliorated determined decreased rate apoptosis, caspase‑3 Bcl‑2/Bax. conclusion, may alleviate OGD/R‑induced injury upregulating SIRT1 PGC‑1α expression, reducing excessive overactivation mitophagy.
Language: Английский
Citations
2
MedComm, Journal Year: 2025, Volume and Issue: 6(3)
Published: Feb. 24, 2025
ABSTRACT Programmed cell death, including necroptosis, plays a critical role in the pathogenesis of cerebral ischemia/reperfusion injury (CIRI). Silent information regulator 1 (SIRT1) has been identified as potential therapeutic target for CIRI, yet its precise regulating necroptosis remains controversial. Furthermore, interaction between SIRT1 and receptor‐interacting protein kinase (RIP1) this context is not fully understood. Sanpian Decoction (SPD), classical traditional herbal formula, was previously shown to enhance expression our studies. Our findings demonstrated that, both vivo vitro, CIRI associated with decrease levels phosphorylated dynamin‐related (p‐DRP1) at Ser637, alongside an increase RIP1 other necroptosis‐related proteins. Co‐immunoprecipitation immunofluorescence analyses revealed weakened RIP1. abnormal mitochondrial fission dysfunction were mediated through phosphoglycerate mutase 5–DRP1 pathway. Notably, SPD treatment improved neurological outcomes reversed these pathological changes by enhancing SIRT1–RIP1 interaction. In conclusion, study suggests that promising capable inhibiting mitigating via exhibits activating SIRT1, thereby attenuating during CIRI.
Language: Английский
Citations
1
International Journal of Nanomedicine, Journal Year: 2024, Volume and Issue: Volume 19, P. 1431 - 1450
Published: Feb. 1, 2024
Introduction: Basic fibroblast growth factor (bFGF) shows great potential for preventing vascular dementia (VD). However, the blood‒brain barrier (BBB) and low bioavailability of bFGF in vivo limit its application. The present study investigated how nasal administration bFGF-loaded nanoliposomes (bFGF-lips) affects impaired learning cognitive function VD mice underlying mechanism involved. Methods: A mouse model was established through repeated cerebral ischemia‒reperfusion. Morris water maze (MWM) novel object recognition (NOR) tests were performed to assess mice. Hematoxylin eosin (HE) staining, Nissl staining TUNEL used evaluate histopathological changes each group. ELISA Western blot analysis investigate molecular by which bFGF-lips improve incidence. Results: Behavioral analyses showed that significantly improved group compared groups; addition, abnormalities apoptosis indices hippocampal neurons decreased. revealed increased concentrations superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), bFGF, B-cell lymphoma 2 (Bcl-2), phosphorylated protein kinase B (PAKT), nuclear erythroid 2-related (Nrf2), NAD(P)H quinone oxidoreductase 1 (NQO1) haem oxygenase-1 (HO-1) hippocampus with groups. Furthermore, malondialdehyde (MDA), caspase-3 2-associated X (Bax) clearly lower than Conclusion: This confirmed hippocampi treatment reduced I/R-induced neuronal regulating apoptosis-related activating phosphatidylinositol-3-kinase (PI3K)/(AKT)/Nrf2 signaling pathway inhibit oxidative stress. Keywords: nanoliposomes, dementia, administration, stress,
Language: Английский
Citations
4
Journal of Biochemical and Molecular Toxicology, Journal Year: 2025, Volume and Issue: 39(2)
Published: Jan. 26, 2025
Ischemia-reperfusion (I/R) injury is a significant clinical problem impacting the heart and other organs, such as kidneys liver. This study explores protective effects of oxycodone on myocardial I/R its underlying mechanisms. Using model in Sprague-Dawley (SD) rats an oxygen-glucose deprivation/reoxygenation (OGD/R) H9c2 cells, we administered inhibited AMP-activated protein kinase (AMPK) with Compound C (C.C). Our results showed that significantly reduced lactate dehydrogenase (LDH) release reactive oxygen species (ROS) production while stabilizing mitochondrial membrane potential (MMP). Western blot RT-qPCR analyzes confirmed enhances AMPK phosphorylation upregulates expression Silent Information Regulator 1 (SIRT1) Peroxisome Proliferator-Activated Receptor γ Coactivator 1α (PGC-1α), thereby protecting cells. These findings suggest exerts against by activating pathway, offering new therapeutic targets for protection.
Language: Английский
Citations
0
Chemico-Biological Interactions, Journal Year: 2025, Volume and Issue: unknown, P. 111405 - 111405
Published: Jan. 1, 2025
Language: Английский
Citations
0
Phytomedicine, Journal Year: 2025, Volume and Issue: 140, P. 156626 - 156626
Published: March 9, 2025
Upon cerebral ischemia/reperfusion injury (CIRI), the brain tissue experiences excessive inflammatory responses, which fuel activation of immune cells, thereby intensifying cellular damage and reactions. Naoqing formula (NQ), a traditional Chinese medicinal compound formulated with musk as primary component, has been extensively utilized in China for clinical treatment ischaemic stroke (IS). The precise pharmacological mechanism underlying NQ's efficacy managing IS remains elusive. In this study, we investigate protective effect molecular NQ against CIRI. C57BL/6 mice were to effects (130, 260 520mg/kg) middle artery occlusion (MCAO) induced CIRI mechanism. Employing biology techniques, transcriptomics, proteomics, network analyses, study assessed role response neuronal cells by establishing model cell microglia oxygen-glucose deprivation/reperfusion (OGD/R) lipopolysaccharide (LPS) stimulation. demonstrated significant mitigating infarction CIRI, achieved through enhancement cortical blood flow. Transcriptomic analyses revealed that mitigated caused modulating Csf3-mediated JAK/STAT pathway. Proteomic analysis further corroborated finding, indicating reduced impact regulating macrophage polarization. Notably, treated NQ, there was notable downregulation Csf3, JAK2, STAT3, STAT6, along co-localization Csf3 CD206. These observations suggested inhibited pathway exerted its anti-inflammatory orchestrating transition macrophages from M1 phenotype M2 phenotype, triggered Csf3. Consistent vivo findings, also microglial polarization vitro, protecting OGD/R- LPS-induced injury. This confirmed prevented inhibiting provided new perspective on use IS.
Language: Английский
Citations
0
Stem Cell Research & Therapy, Journal Year: 2025, Volume and Issue: 16(1)
Published: May 1, 2025
Language: Английский
Citations
0
Journal of Neuropathology & Experimental Neurology, Journal Year: 2024, Volume and Issue: unknown
Published: Aug. 19, 2024
Abstract Ischemic stroke is a major cause of global death and permanent disability. Major consequences ischemic include neuronal mitochondrial dysfunction. We investigated the effects senescence marker protein 30 (SMP30) on mitochondria-mediated apoptosis histone deacetylase 4 (HDAC4)/postsynaptic density-95 (PSD-95) signaling in models vivo vitro. Rats with middle cerebral artery occlusion/reperfusion (MCAO/R) were used to simulate ischemia/reperfusion (I/R) injury. SMP30 was downregulated brain tissues rats after I/R induction. overexpression decreased MCAO/R-induced infarct volumes improved neurologic function histopathological changes. Increasing expression suppressed reduced SH-SY5Y PC12 cells treated oxygen-glucose deprivation/reoxygenation (OGD/R) HDAC4 PSD-95 expression; could bind HDAC4. Furthermore, upregulation abolished OGD/R-induced dysfunction cells. Together, these findings indicate that alleviates I/R-induced injury by inhibiting HDAC4/PSD-95 preserve function. These interactions might provide new treatment methods for patients stroke.
Language: Английский
Citations
1
Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 486, P. 137001 - 137001
Published: Dec. 26, 2024
Language: Английский
Citations
1
Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)
Published: Oct. 26, 2024
Language: Английский
Citations
0