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

LncRNA Peg13 Alleviates Myocardial Infarction/Reperfusion Injury through Regulating MiR-34a/Sirt1-Mediated Endoplasmic Reticulum Stress DOI Open Access
Yonghong Wang, Jian Luo, Huiqiong Yang

et al.

International Heart Journal, Journal Year: 2024, Volume and Issue: 65(3), P. 517 - 527

Published: May 30, 2024

Myocardial infarction/reperfusion (I/R) injury significantly impacts the health of older individuals. We confirmed that level lncRNA Peg13 was downregulated in I/R injury. However, detailed function myocardial has not yet been explored.To detect Peg13, vivo model constructed. RT-qPCR employed to investigate RNA levels, and Western blotting performed assess levels endoplasmic reticulum stress apoptosis-associated proteins. EdU staining cell proliferation.I/R therapy dramatically produced injury, increased infarct area, decreased amount tissues mice. In addition, hypoxia/reoxygenation (H/R) notably induced apoptosis promoted (ER) HL-1 cells, while overexpression reversed these phenomena. Additionally, may increase Sirt1 through binding miR-34a. Upregulation H/R-induced ER via regulation miR-34a/Sirt1 axis.LncRNA reduces mediation axis. Hence, our research might shed new lights on developing strategies for treatment

Language: Английский

Citations

0
Neuroprotective potential for mitigating ischemia-reperfusion-induced damage DOI Creative Commons
Zi Ye,

R Liu,

Hang‐Xing Wang

et al.

Neural Regeneration Research, Journal Year: 2024, Volume and Issue: 20(8), P. 2199 - 2217

Published: July 29, 2024

Reperfusion following cerebral ischemia causes both structural and functional damage to brain tissue could aggravate a patient’s condition; this phenomenon is known as ischemia-reperfusion injury. Current studies have elucidated the neuroprotective role of sirtuin protein family (Sirtuins) in modulating However, potential utilizing it novel intervention target influence prognosis injury requires additional exploration. In review, origin research progress Sirtuins are summarized, suggesting involvement diverse mechanisms that affect injury, including inflammation, oxidative stress, blood–brain barrier damage, apoptosis, pyroptosis, autophagy. The therapeutic avenues related may improve were also investigated by expression affecting representative pathways, such nuclear factor-kappa B signaling, stress mediated adenosine monophosphate-activated kinase, forkhead box O. This review summarizes endogenous substances, RNA hormones, drugs, dietary supplements, emerging therapies regulate expression. reveals regulating mitigates when combined with other risk factors. While show promise for treatment most recent based on rodent models circadian rhythms distinct from those humans, potentially influencing efficacy Sirtuins-targeting drug therapies. Overall, provides new insights into pathology

Language: Английский

Citations

0
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

Citations

0