المؤلفون: Lu Yu, Zuohui Zhang, Hao Chen, Miao Wang, Wenqi Mao, Jinxia Hu, Dandan Zuo, Bingchen Lv, Weifeng Wu, Suhua Qi, Guiyun Cui

المصدر: Bioengineering & Translational Medicine, Vol 8, Iss 6, Pp n/a-n/a (2023)

مصطلحات موضوعية: acute ischemic stroke, high throughput screening, microglial, pyroptosis, remote limb ischemic postconditioning, Chemical engineering, TP155-156, Biotechnology, TP248.13-248.65, Therapeutics. Pharmacology, RM1-950

الوصف: Abstract The repetitive inflation–deflation of a blood pressure cuff on a limb is known as remote limb ischemic postconditioning (RIPostC). It prevents brain damage induced by acute ischemia stroke (AIS). Pyroptosis, executed by the pore‐forming protein gasdermin D (GSDMD), is a type of regulated cell death triggered by proinflammatory signals. It contributes to the pathogenesis of ischemic brain injury. However, the effects of RIPostC on pyroptosis following AIS remain largely unknown. In our study, linear correlation analysis confirmed that serum GSDMD levels in AIS patients upon admission were positively correlated with NIHSS scores. RIPostC treatment significantly reduced GSDMD level compared with patients without RIPostC at 3 days post‐treatment. Besides, middle cerebral artery occlusion (MCAO) surgery was performed on C57BL/6 male mice and RIPostC was induced immediately after MCAO. We found that RIPostC suppressed the activation of NLRP3 inflammasome to reduce the maturation of GSDMD, leading to decreased pyroptosis in microglia after AIS. Hepatocyte growth factor (HGF) was identified using the high throughput screening. Importantly, HGF siRNA, exogenous HGF, and ISG15 siRNA were used to reveal that HGF/ISG15 is a possible mechanism of RIPostC regulation in vivo and in vitro.

وصف الملف: electronic resource

العلاقة: https://doaj.org/toc/2380-6761Test

الوصول الحر: https://doaj.org/article/798bf6e67cd64807b2ef1f003cad09e2Test

المؤلفون: Hulya Karatas

المصدر: Frontiers in Cellular Neuroscience, Vol 17 (2023)

مصطلحات موضوعية: ischemic postconditioning, gliomas, febrile seizure, xenon treatment, intracerebral hemorrhage, NADPH oxidase 4, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571

وصف الملف: electronic resource

العلاقة: https://www.frontiersin.org/articles/10.3389/fncel.2023.1327072/fullTest; https://doaj.org/toc/1662-5102Test

الوصول الحر: https://doaj.org/article/a8b41f2f81bf44948244518db551816bTest

المؤلفون: Takeuchi, Toshiharu¹ (AUTHOR), Hasebe, Naoyuki¹ (AUTHOR)

المصدر: Journal of the American College of Cardiology (JACC). 2024 Supplement, Vol. 83 Issue 13, p1199-1199. 1p.

مصطلحات موضوعية: *MYOCARDIAL infarction, *ISCHEMIC postconditioning, *ANGINA pectoris

المؤلفون: Perez, V.¹ (AUTHOR), Zaobornyj, T.^1,2 (AUTHOR), Vico, T.^1,2 (AUTHOR), Vanasco, V.^1,2 (AUTHOR), Marchini, T.^1,2 (AUTHOR), Godoy, E.¹ (AUTHOR), Alvarez, S.^1,2 (AUTHOR), Evelson, P.^1,2 (AUTHOR), Donato, M.¹ (AUTHOR), Gelpi, R.J.¹ (AUTHOR), D'Annunzio, V.¹ (AUTHOR) vdannunzio@fmed.uba.ar

المصدر: Archives of Biochemistry & Biophysics. Mar2024, Vol. 753, pN.PAG-N.PAG. 1p.

مصطلحات موضوعية: *TRANSGENIC mice, *ISCHEMIC postconditioning, *MICE, *HYDROGEN peroxide, *MIDDLE age, *NITRATION

مستخلص: Thioredoxin-1 (Trx1) has cardioprotective effects on ischemia/reperfusion (I/R) injury, although its role in ischemic postconditioning (PostC) in middle-aged mice is not understood. This study aimed to evaluate if combining two cardioprotective strategies, such as Trx1 overexpression and PostC, could exert a synergistic effect in reducing infarct size in middle-aged mice. Young or middle-aged wild-type mice (Wt), transgenic mice overexpressing Trx1, and dominant negative (DN-Trx1) mutant of Trx1 mice were used. Mice hearts were subjected to I/R or PostC protocol. Infarct size, hydrogen peroxide (H 2 O 2) production, protein nitration, Trx1 activity, mitochondrial function, and Trx1, pAkt and pGSK3β expression were measured. PostC could not reduce infarct size even in the presence of Trx1 overexpression in middle-aged mice. This finding was accompanied by a lack of Akt and GSK3β phosphorylation, and Trx1 expression (in Wt group). Trx1 activity was diminished and H 2 O 2 production and protein nitration were increased in middle-age. The respiratory control rate dropped after I/R in Wt-Young and PostC restored this value, but not in middle-aged groups. Our results showed that Trx1 plays a key role in the PostC protection mechanism in young but not middle-aged mice, even in the presence of Trx1 overexpression. [Display omitted] • Postconditioning and Trx-1 overexpression cannot reduce infarction in middle age. • Postconditioning and Trx-1 overexpression trigger similar intracellular mechanisms. • In middle age, a redox imbalance takes place. [ABSTRACT FROM AUTHOR]

المؤلفون: Ma, Wei¹ (AUTHOR), Yang, Jinwei^1,2 (AUTHOR), Zhang, Jinfen¹ (AUTHOR), He, Rui¹ (AUTHOR), Luo, Yi¹ (AUTHOR), Li, Chunyan^1,3 (AUTHOR), Zhao, Feng¹ (AUTHOR), Tao, Fengping¹ (AUTHOR), Fan, Jingjing¹ (AUTHOR), Yin, Luwei¹ (AUTHOR), Zhu, Kewei¹ (AUTHOR), Niu, Shourui¹ (AUTHOR), Li, Liyan¹ (AUTHOR) kmliyanl@163.com

المصدر: Brain Research. Feb2024, Vol. 1824, pN.PAG-N.PAG. 1p.

مصطلحات موضوعية: *ISCHEMIC postconditioning, *ISCHEMIC stroke, *STROKE patients, *CELLULAR signal transduction, *CEREBRAL infarction

مستخلص: [Display omitted] • The rat models of ischemic cerebral stroke with ISP and RIP were established. • RIP had cerebral protective effects for the ischemic stroke rats. • TGFβ1 and Smad2/3 was related to cerebral protection of ischemic postconditioning. Patients with acute ischemic stroke achieve inadequate benefit due to the short therapeutic window for thrombolysis and the risk of ischemia/reperfusion (IR) injury. Ischemic postconditioning induces endogenous cerebral protection for acute ischemic stroke, although the protective mechanisms associated with ischemic postconditioning haven't been well clarified. In present study, the rat models of ischemic cerebral stroke with in situ and remote ischemic postconditioning (ISP and RIP) were established successfully. The Zea Longa and the modified neurological severity scoring (mNSS) were carried out to evaluate neurological function in the rats, while the open field test was explored to estimate their autonomic athletic ability. The 2,3,5-riphenyltetrazolium chloride (TTC) staining method was used to measure the size of the infarcts. TUNEL and Nissl's staining were used to detect the apoptosis rate of cells in the ischemic penumbra, with the expression of TGFβ1, Smad2, and Smad3 in the ischemic penumbra and serum detected by immunohistochemical staining, qRT-PCR, Western blots, and ELISA analysis. We showed that application of both types of ischemic postconditioning had cerebral protective effects for the ischemic stroke rats, that included effective reduction in the volume of cerebral infarction, alleviation of apoptosis and inflammation in the ischemic penumbra, and promotion of recovery of neurological function. These effects included significantly enriched gene ontology (GO) terms after RIP intervention that were related to TGFβ1, increased protein levels of TGFβ1 and decreased levels of p-Smad2/3 and smad3 following RIP intervention. We showed that the TGFβ1-Smad2/3 signaling pathway was associated with the cerebral protection of ischemic postconditioning. [ABSTRACT FROM AUTHOR]

المؤلفون: Chen, Gangling^1,2 (AUTHOR), Zhang, Jiangwei^1,2 (AUTHOR), Sheng, Mingyue^1,2 (AUTHOR), Zhang, Sanli^1,2 (AUTHOR), Wu, Qi³ (AUTHOR), Liu, Lei⁴ (AUTHOR), Yu, Boyang^1,2 (AUTHOR), Kou, Junping^1,2 (AUTHOR) junpingkou@cpu.edu.cn

المصدر: Redox Report. Dec 2021, Vol. 26 Issue 1, p176-183. 8p.

مصطلحات موضوعية: *NEUTROPHILS, *ISCHEMIC postconditioning, *MYOCARDIAL reperfusion, *REACTIVE oxygen species, *GENE expression, *SPRAGUE Dawley rats, *TUMOR necrosis factors

مستخلص: The study explores the protective role of the peripheral serum of limb remote ischemic postconditioning (LRIP) in reducing the reactive oxygen species (ROS) levels and neutrophil activation, which are responsible for the deleterious reperfusion injury. LRIP was induced in Sprague–Dawley rats by three cycles of 5 min occlusion /5 min reperfusion on the left hind limb. The blood samples were collected before LRIP or 0 and 1 h after LRIP (named SerumSham, SerumLRIP0, SerumLRIP1, respectively). The effects of LRIP serum on ROS level and neutrophils activation were determined. The expression of MyD88-TRAF6-MAPKs and PI3K/AKT pathways in neutrophils were examined. When compared with SerumSham, SerumLRIP0 and SerumLRIP1 significantly reduced the ROS released from neutrophils activated by fMLP. Meanwhile, the mRNA expression levels of NADPH oxidase subunit p22phox and multiple ROS-producing related key proteins, such as NADPH oxidase subunit p47phox ser 304, ser 345. MyD88, p-ERK, p-JNK and p-P38 expression of neutrophils were downregulated by SerumLRIP0 and SerumLRIP1. SerumLRIP1 also downregulated p47phox mRNA expression and tumor necrosis factor receptor-associated factor 6 (TRAF6) protein expression. LRIP serum protects against ROS level and neutrophils activation involving the MyD88-TRAF6-MAPKs. This finding provides new insight into the understanding of LRIP mechanisms. [ABSTRACT FROM AUTHOR]

المؤلفون: Tahamtan, Mahshid¹, Nazari, Abbas², Aghaei, Iraj³, Shabani, Mohammad⁴ shabanimoh@yahoo.com

المصدر: Basic & Clinical Neuroscience. Nov/Dec2021, Vol. 12 Issue 6, p1-40. 40p.

مصطلحات موضوعية: *BRAIN-derived neurotrophic factor, *ISCHEMIC postconditioning, *COGNITION disorders, *OPERANT conditioning, *ACUTE kidney failure, *NEPHRECTOMY, *MYOCARDIAL reperfusion

مستخلص: Background and aim: Acute kidney injury (AKI) is a frequent complication of kidney failure with high mortality which leads to brain dysfunction. The aim of this study was to investigate the possible protective effect of ischemic postconditioning (IPo) against brain dysfunction induced by bilateral renal ischemia (BRI). Materials and methods: Male Wistar rats underwent BRI, sham or IPo surgery 24h and 1w after reperfusion. Explorative behaviors and motor function of the rats was evaluated by open field, rotarod and wire grip tests. The cognitive function was assessed by passive avoidance learning and Morris water maze tests. Western blotting was performed to assess hippocampal brain derived neurotrophic factor (BDNF) expression. Results: Impairment of balance function induced by BRI was not reversed but Passive avoidance learning impairment was reversed by postconditioning 24h after reperfusion. IPo increased muscle strength compared to BRI group, but explorative behaviors and balance function had no difference 1w after reperfusion. BRI decreased significantly the BDNF protein expression in the hippocampus and postconditioning increased that 24h after reperfusion. Conclusion: Results demonstrated deleterious effect of BRI on cognitive and balance function 24h after reperfusion. IPo showed curative effect against cognitive dysfunction probably through enhancement of BDNF protein expression in the hippocampus. [ABSTRACT FROM AUTHOR]

المؤلفون: Zhao, Ling¹ (AUTHOR), Tan, Shufen² (AUTHOR), Liao, Qiwei³ (AUTHOR), Li, Xia⁴ (AUTHOR), Ke, Tingyu¹ (AUTHOR), Li, Shuqing⁴ (AUTHOR) shuqing28@hotmail.com

المصدر: Brain & Behavior. Nov2021, Vol. 11 Issue 11, p1-9. 9p.

مصطلحات موضوعية: *ISCHEMIC stroke, *ISCHEMIC postconditioning, *CELLULAR signal transduction, *NEUROPROTECTIVE agents, *DIABETES, *MYOCARDIAL reperfusion

مستخلص: Introduction: Patients with comorbidity of ischemic stroke (IS) and diabetes mellitus (DM) show poor neurological functional recovery, and ischemic postconditioning (IPOC) should be considered a powerful neuroprotective method for IS. However, whether it should be introduced for patients with IS and DM remains controversial. This study established a DM with IS (DMIS) tree shrew model, which was intervened by IPOC to assess its neuroprotective effects and also to analyze the relevant mechanism by RNA‐sequence and bioinformatics analysis. Methods: Fifty‐four tree shrews were randomly divided into a sham operation control group, a DMIS group, and an IPOC group (DMIS model), with 18 tree shrews per group. Triphenyl tetrazolium chloride (TTC), hematoxylin‐eosin (HE) staining, transmission electron microscopy (TEM), and RNA‐sequence analysis were performed to assess the IPOC effect. Results: IPOC reduced infarct size and reduced nerve cell injury in IS tree shrews with DM. RNA‐seq analysis showed that IPOC significantly increased the expression of the homeobox protein SIX3, while downregulating the expression of HLA class II histocompatibility antigens DQ beta 1 chain, CAS1 domain‐containing protein 1, and cytokine receptor‐like factor 2. The most downregulated signaling pathways include the NF‐κB signaling pathway, TNF signaling pathway, and Fc gamma R‐mediated phagocytosis. Conclusions: IPOCs have a neuroprotective effect in a DMIS animal model that reduces infarct size and nerve cell injury. This mechanism might be related to reducing inflammation and stress responses that decreases the activity of TNF and NF‐κB signaling pathways. [ABSTRACT FROM AUTHOR]

المؤلفون: Jia, Degong¹ (AUTHOR), Pan, Qi² (AUTHOR), Zhang, Yijie² (AUTHOR), Yu, Yang² (AUTHOR), Song, Zhanyu² (AUTHOR), Liu, Yong feng² (AUTHOR), Jia, Zhixing¹ (AUTHOR), Guo, Shanshan³ (AUTHOR), Cheng, Ying² (AUTHOR) chengying75@sina.com

المصدر: Clinical Transplantation. Oct2021, Vol. 35 Issue 10, p1-9. 9p.

مصطلحات موضوعية: *ISCHEMIC postconditioning, *LIVER transplantation, *ORGAN donors, *BILE ducts, *INTERNATIONAL normalized ratio

مصطلحات جغرافية: ALABAMA

مستخلص: Aim: This study investigated whether ischemic postconditioning (IPO) improved the outcome of organs from donors after cardiac death and had a synergistic effect with hypothermic machine perfusion (HMP) in a pig liver transplantation model. Methods: A donor after cardiac death (DCD) model was developed in 48 healthy Bama miniature pigs randomly divided into four groups: simple cold storage group (SCS group), IPO group, HMP group, HMP–IPO group. The levels of serum alanine aminotransferase (ALT), total bilirubin, histopathological findings, apoptotic activity of hepatocytes, international normalized ratio (INR), tumor necrosis factor‐α (TNF‐α), and Malondialdehyde (MDA) were compared. Results: All recipients in the SCS group died within 6 h after transplantation. The livers of the recipients in the IPO had 50% survival on day 5. HMP allowed 83.3% survival and HMP–IPO allowed 100% survival. After reperfusion, the recipients in the IPO and HMP–IPO group had lower ALT and total bilirubin levels, less Suzuki score, less apoptosis, and less injury to hepatocytes and biliary ducts and attenuated inflammatory response and oxidative load. Conclusions: IPO improved the outcome of organs from donors after cardiac death and had a synergistic effect with HMP in the pig liver transplantation model. [ABSTRACT FROM AUTHOR]

المؤلفون: Jorge Nuche, Carlos Galán-Arriola, Rodrigo Fernández-Jiménez, María Isabel Higuero Verdejo, Victoria I. González Pastor, Ravi Vazirani, Arturo Lanaspa, María Anguita-Gámez, Gonzalo J. López Martín, Javier Sánchez-González, Borja Ibáñez

المصدر: REC: Interventional Cardiology (English Ed.), Vol 5, Iss 1, Pp 29-37 (2023)

مصطلحات موضوعية: Reperfusion injury, Ischemic postconditioning, Cardioprotection, Myocardial infarction, Medicine

الوصف: ABSTRACT Introduction and objectives: Ischemic postconditioning (iPost, coronary intermittent re-occlusion maneuvers immediately after PCI-mediated reperfusion) has been proposed to limit infarct size (IS). However, a few experimental and clinical contradictory results have been reported. We hypothesized that iPost cardioprotection is affected by the duration of ischemia. Our objective was to assess IS in the presence/absence of iPost in a pig model of myocardial infarction of variable ischemia duration. Methods: Large white pigs (n = 38) underwent angioplasty balloon-induced coronary ischemia followed by reperfusion. Two set of experiments were carried out: intermediate (30 min) and prolonged (40 min) ischemia. In both, pigs were allocated on a 1:1 ratio to receive iPost (4 cycles of “1 min balloon inflation followed by 1 min deflation” upon reperfusion) or control. Animals underwent contrast-enhanced multiparametric cardiac magnetic resonance scan on day 7. Primary outcome measure was cardiac magnetic resonance-based IS (% of left ventricular mass). The interaction between treatment allocation and ischemia duration was assessed using a 2-way ANOVA test. Results: iPost was not associated with smaller IS in any of the ischemia duration protocols (intermediate ischemia: 0.3% [0.0–3.9] vs 0.9% [0.0–2.6] in iPost and control, respectively; P = .378; long ischemia: 31.1% [27.3–32.8] vs 27.3% [25.1–27.5]; P = .248). When both ischemia-duration protocols were combined, iPost was not associated with smaller IS (3.9% [0.0–30.9] vs 4.6% [0.2–25.1]; P = .672). T1 relaxation times were longer in animals undergoing iPost compared to controls (1306.2 ms [1190.7–1492.7] vs 1240.7 ms [1167.1–1304.5]; P = .024). Conclusions: In a pig model of reperfused myocardial infarction of variable ischemia duration, iPost failed to reduce IS. T1 relaxation times were longer in animals undergoing iPost indicative of the potential harm involved in this procedure.

وصف الملف: electronic resource

العلاقة: https://recintervcardiol.org/en/index.php?option=com_content&view=article&id=978Test; https://doaj.org/toc/2604-7322Test

الوصول الحر: https://doaj.org/article/b23339763b38448cabac0c5966ddb3c7Test