Remote Ischemic Preconditioning Plays a Neuroprotective Role in Cerebral Ischemia-Reperfusion Mice by Inhibiting Mitophagy DOI Creative Commons
Jiayi Zhu, Na Xu,

Heng Lin

et al.

Heliyon, Journal Year: 2024, Volume and Issue: 10(20), P. e39076 - e39076

Published: Oct. 1, 2024

Remote ischemic preconditioning (RIPC) represents a clinically feasible method for safeguarding vital organs against injury. However, its specific role in cerebral ischemia-reperfusion (I/R) injury remains to be definitively elucidated. In this study, we investigated the neuroprotective effects of RIPC on mice at 7 days post-cerebral I/R and involvement mitophagy mitochondrial dysfunction. Cerebral led impaired brain function, as well structural functional damage mitochondria. Notably, treatment ameliorated neurological dysfunction induced by I/R. Compared with group, expression levels NeuN, MBP, PDH, Tom20 were significantly elevated RIPC+I/R group. Furthermore, mitochondria group exhibited more intact structure compared those subjected injury, markedly increased ATP content, ADP TAN level glucose uptake while upregulating Parkin, Pink1 P62 proteins; it also reduced both volume foci number autophagosomes along decreasing LC3B II/I ratio. conclusion, may exert inhibiting excessive during subacute stages following an stroke.

Language: Английский

E2F1/CDK5/DRP1 axis mediates microglial mitochondrial division and autophagy in the pathogenesis of cerebral ischemia‐reperfusion injury DOI Creative Commons

Yongpeng Yuan,

Tingting Chen, Yanling Yang

et al.

Clinical and Translational Medicine, Journal Year: 2025, Volume and Issue: 15(2)

Published: Feb. 1, 2025

Language: Английский

Citations

1
The SIRT-1/Nrf2/HO-1 Axis: Guardians of Neuronal Health in Neurological Disorders DOI
Pranshul Sethi, Sidharth Mehan, Zuber Khan

et al.

Behavioural Brain Research, Journal Year: 2024, Volume and Issue: unknown, P. 115280 - 115280

Published: Oct. 1, 2024

Language: Английский

Citations

4
USP7 promotes PINK1/Parkin-dependent mitophagy to ameliorate cerebral ischemia–reperfusion injury by deubiquitinating and stabilizing SIRT1 DOI
Dan Hou, Yujie Hu,

Yun Tian

et al.

Brain Research, Journal Year: 2025, Volume and Issue: unknown, P. 149638 - 149638

Published: April 1, 2025

Language: Английский

Citations

0
Role of sirtuins in cerebral ischemia-reperfusion injury: Mechanisms and therapeutic potential DOI Creative Commons
Zheng Li, Jihong Xing

International Journal of Biological Macromolecules, Journal Year: 2025, Volume and Issue: 310, P. 143591 - 143591

Published: April 27, 2025

The high incidence and mortality rate of cardiac arrest (CA) establishes it as a critical clinical challenge in emergency medicine globally. Despite continuous advances advanced life support (ALS) technology, the prognosis for patients experiencing remains poor, with cerebral ischemia reperfusion injury (CIRI) being significant determinant adverse neurological outcomes increased mortality. Sirtuins (SIRTs) are class highly evolutionarily conserved NAD+-dependent histone deacylenzymes capable regulating expression various cytoprotective genes to play neuroprotective role CIRI. SIRTs mainly regulate levels downstream proteins such PGC 1-α, Nrf 2, NLRP 3, FoxOs, PINK 1 inhibit inflammatory response, attenuate oxidative stress, improve mitochondrial dysfunction, promote angiogenesis, apoptosis while reducing Natural active ingredients widely used protein level body because their multi-components, multi-pathway, multi-target, minimal toxic side effects. However, these naturally still face many challenges related drug targeting, pharmacokinetic properties, delivery. emergence vigorous development new delivery systems, nanoparticles, micromilk, exosomes, provide strong solving above problems. In context rapid molecular biology non-coding RNA (NcRNA), represented by miRNA LncRNA, offers great potential achieving gene-level precision medicine. multidisciplinary integration, combining biotechnology, omics technologies, artificial intelligence, material science will strongly deepening basic research expand application. This review describes major signaling pathways targeting mitigate CIRI, well current status Chinese Western medical means intervention SIRTs. Meanwhile, possible solutions application targeted drugs summarized. industrial crossover, direction future is discussed valuable reference researchers clinicians diagnosis treatment effects

Language: Английский

Citations

0
RCN2 promotes Nasopharyngeal carcinoma progression by curbing Calcium flow and Mitochondrial apoptosis DOI Creative Commons
Hui Yao, Siyu Zhang,

Haijing Xie

et al.

Cellular Oncology, Journal Year: 2023, Volume and Issue: 46(4), P. 1031 - 1048

Published: March 23, 2023

Abstract Objective Evidence suggests that calcium release from the endoplasmic reticulum (ER) can be induced to cause overload, which in turn trigger mitochondrial-dependent apoptosis. Dysregulation of systemic homeostasis and changing levels calcium-binding proteins have been shown associated with malignant behavior tumors. However, precise molecular mechanism underlying Nasopharyngeal carcinoma (NPC) remains uncertain. Methods Reticulocalbin (RCN2) expression NPC was assessed using GEO database, western blot analysis qRT-PCR. Apoptosis flow cytometric apoptosis-related were determined analysis. Intracellular ion concentrations measured fluorescence imaging. The findings these analyses validated vitro nude mice models. Luciferase ChIP assays used measure transcriptional regulation. Clinical significance evaluated tissue microarray (n=150). Results Our results showed RCN2 promotes malignancy by causing Ca2+ imbalance, leads initiation stress-mediated mitochondrial apoptosis pathway. We demonstrate calreticulin (CALR) resides primarily interacts RCN2. Moreover, transcription factors YY1 homeobox protein goosecoid (GSC) both contribute directly binding predicted promoter region Finally, high combined GSC may serve as an important clinical biomarker poor prognosis patients NPC. Conclusion are upstream regulators RCN2, involved overload stress-induced Thus, they play significant role development NPCs.

Language: Английский

Citations

8
Molecular aspects of optic nerve autophagy in glaucoma DOI Creative Commons
Yasushi Kitaoka, Kana Sase

Molecular Aspects of Medicine, Journal Year: 2023, Volume and Issue: 94, P. 101217 - 101217

Published: Oct. 14, 2023

The optic nerve consists of the glia, vessels, and axons including myelin axoplasm. Since axonal degeneration precedes retinal ganglion cell death in glaucoma, preceding model may be helpful for understanding molecular mechanisms degeneration. Optic samples from these models can provide information on several aspects autophagy. Autophagosomes, most typical organelles expressing autophagy, are found much more frequently inside than around glia. Thus, immunoblot findings reflect autophagy state axons. Autophagic flux impairment occur degenerating axons, as other central nervous system neurodegenerative diseases. Several candidates involved enhancement, leading to protection. This concept is an attractive approach prevention further death. In this review, we describe factors affecting nicotinamide riboside, p38, ULK, AMPK, ROCK, SIRT1, propose potential methods protection via enhancement

Language: Английский

Citations

5
Metabolomics-Based Study of the Protective Effect of 4-Hydroxybenzyl Alcohol on Ischemic Astrocytes DOI Open Access
Tian Xiao,

Xingzhi Yu,

Jie Tao

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(18), P. 9907 - 9907

Published: Sept. 13, 2024

Ischemic stroke is a common and dangerous disease in clinical practice. Astrocytes (ASs) are essential for maintaining the metabolic balance of affected regions during process. 4-Hydroxybenzyl alcohol (4HBA) from

Language: Английский

Citations

1
Targeting sirtuins in neurological disorders: A comprehensive review DOI

Sen-Yu Zhang,

Ni Yang,

Peng-Hui Hao

et al.

International Journal of Biological Macromolecules, Journal Year: 2024, Volume and Issue: 292, P. 139258 - 139258

Published: Dec. 28, 2024

Language: Английский

Citations

1
HSP90β regulates EAAT2 expression and participates in ischemia‑reperfusion injury in rats DOI Creative Commons
Liang Tao, Xiaolin Hu,

Zeng Ling

et al.

Molecular Medicine Reports, Journal Year: 2023, Volume and Issue: 29(1)

Published: Nov. 15, 2023

Cerebrovascular diseases (CVDs) have become a global public health problem and ischemia‑reperfusion injury, the major cause of neurological impairment exacerbation, is closely related to excitotoxicity. The present study aimed investigate effects changes in heat shock protein (HSP)90β expression verify whether HSP90β regulates EAAT2 cerebral injury model. Healthy adult Sprague‑Dawley (SD) male rats were used establish control group, sham‑operated middle artery occlusion (MCAO) empty virus group lentivirus group. A model was established using MCAO method. Lentivirus construction injection interfere with HSP90β. modified severity score assess deficits. Triphenyltetrazolium chloride staining detect infarct areas. Immunofluorescence localization levels determined western blotting reverse transcription‑quantitative PCR. An successfully it found that HSP90β, but not HSP90α, upregulated after MCAO. coincided astrocyte markers ischemic penumbra area, while no observed microglia. Inhibition improved deficits alleviated brain by increasing expression. These results suggested involved process inhibition increases levels, conferring neuroprotective effect rats.

Language: Английский

Citations

2
Rhodiola rosea glycosides modulate ERβ/BNIP3-mediated mitochondrial autophagy in cerebral ischemic neuroprotection DOI Creative Commons
Xing Rong, Li Yu, Yuan-Jia Yue

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: Feb. 7, 2024

Abstract Objectives: Objective To investigate the neuroprotective effect and mechanism of Rhodiola rosea glycosides(SAL) on cerebral ischemia/reperfusion injury (CIRI) rats through mitochondrial autophagy pathway mediated by estrogen receptor β (ERβ)/B-cell lymphoma-2/adenovirus E1B interacting protein 3 (BNIP3). Methods: 135 SD were divided into OVX model groups (OVX+MCAO/R),estradiol control group (OVX+MCAO/R+E2), ERβ inhibitor (OVX+MCAO/R+SAL+PHTPP), (OVX+MCAO/R+SAL+Mdivi-1), SAL low,medium, high dose (OVX+MCAO/R+SAL). MCAO/R+SAL), middle artery embolism (MCAO/R) was constructed using wire method, reperfusion performed for 24h after 1h ischaemia. Neurological function scoring reperfusion; TTC staining used to detect volume infarction; water content brain tissue determined wet dry gravimetry; permeability blood-brain barrier Evans blue (EB) content; levels oestrogen (E2), superoxide dismutase (SOD) malondialdehyde (MDA) analysed kit; neuron pathology observed ischemic side hematoxylin eosin (HE) staining; damage in Nissl kit. observe neuronal tissue; transmission electron microscopy (TEM) autophagosomes; Western blotting expression autophagy-related proteins, BNIP3, NIX, Beclin-1 LC3. Results: There no statistical difference (P>0.05) Longa score, TTC, content, EB, E2 oxidative stress level, HE, Niehl's Con compared with group, indicating that removal ovaries had subsequent experiments; whereas, there a statistically significant (P<0.05) decrease proteins MCAO/R groups, Mdivi-1 PHTPP played protective role against neural SAL-H group. It indicated exerted nerve injury; whereas two PHTPP, significantly different reversed decreased suggesting may protect cells ERβ-mediated autophagy. Conclusions: Conclusion improve neurological modulating level ERβ/BNIP3-mediated self, providing new way drug development based combined as ischemia.

Language: Английский

Citations

0