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69 results for “Ischemia/reperfusion”
Data from: Non‐invasive treatment of ischemia/reperfusion injury: Effective transmission of therapeutic near‐infrared light into the human brain through soft skin‐conforming silicone waveguides
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Gut microbiota-derived gamma-aminobutyric acid from metformin treatment reduces hepatic ischemia/reperfusion injury by inhibiting ferroptosis
<div>Hepatic ischemia/reperfusion injury (HIRI) is a common and inevitable factor leading to poor prognosis in various liver diseases, making the outcomes of current treatments in the clinic unsatisfactory. Metformin has been demonstrated to be beneficial in alleviating HIRI in recent studies, however, the underpinning mechanism remains unclear. In this study, we found metformin mitigates HIRI-induced ferroptosis through reshaped gut microbiota in mice, which was confirmed by the results of fecal microbiota transplantation treatment but showed the elimination of the beneficial effects when gut bacteria were depleted using antibiotics. Detailedly, through 16S rRNA and metagenomic sequencing, we identified that the metformin-reshaped microbiota was characterized by the increase of gamma-aminobutyric acid (GABA) producing bacteria. This increase was further confirmed by the elevation of GABA synthesis key enzymes, glutamic acid decarboxylase, and putrescine aminotransferase, in gut microbes of metformin-treated mice and healthy volunteers. Furthermore, the benefit of GABA against HIRI-induced ferroptosis was demonstrated in GABA-treated mice. Collectively, our data indicate that metformin can mitigate HIRI-induced ferroptosis by reshaping gut microbiota, with GABA identified as a key metabolite.</div>
Protecting Autologous Free Flaps From Ischemia/Reperfusion Damage With Cold Storage.
ClinicalTrials.gov study NCT06523920. IPD Sharing: NO. Countries: 0. Publications: 25.
Gut microbiota-derived gamma-aminobutyric acid from metformin treatment reduces hepatic ischemia/reperfusion injury by inhibiting ferroptosis
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Figure 2 in Investigation of the effect of silymarin on oxidative DNA damage and inflammatory markers in ischemia/reperfusion injury following experimental testicular torsion/detorsion in rats
Figure 2. Testicular tissue, control group, negative Tnf-α expression (A). T 3 h / D 3 h group: very severe Tnf-α expression in the perivascular and intertubular intervals (arrowheads) (B). T 3 h / D 24 h group: severe Tnf-α expression in the perivascular and intertubular intervals (arrowheads) (C). T 3 h / D 3 h + silymarin group: medium level Tnf-α expression in the perivascular and intertubular intervals (arrowheads) (D). T 3 h / D 24 h + silymarin group: mild Tnf-α expression in the perivascular and intertubular intervals (arrowheads) (E). IHC-P, bar: 50 µm.
Figure 1 in Investigation of the effect of silymarin on oxidative DNA damage and inflammatory markers in ischemia/reperfusion injury following experimental testicular torsion/detorsion in rats
Figure 1. Testicular tissue, control group, normal histological view (A). T 3 h / D 3 h group: necrosis in spermatocytes (arrowheads); severe congestion in intertubular intervals (thick arrows); hemorrhage, thinning in the tubulus wall (B). T 3 h / D 24 h: necrosis in spermatocytes (arrowheads); severe edema in the intertubular space (stars); thinning of the tubulus wall (C). T 3 h / D 3 h + silymarin group: moderate edema in the intertubular intervals (star); congestion (thick arrow) (D). T 3 h / D 24 h + silymarin group: mild edema at intertubular intervals (star) (E); H and E, bar: 50 µm.
Figure 3 in Investigation of the effect of silymarin on oxidative DNA damage and inflammatory markers in ischemia/reperfusion injury following experimental testicular torsion/detorsion in rats
Figure 3. Testicular tissue, control group, negative 8-OHdG expression (A). T 3 h / D 3 h group: severe cytoplasmic 8-OHdG expression in spermatocytes (arrowheads) (B). T 3 h / D 24 h group: severe cytoplasmic 8-OHdG expression in spermatocytes (arrowheads) (C). T 3 h / D 3 h + silymarin group: moderate cytoplasmic 8-OHdG expression in spermatocytes (arrowheads) (D). T 3 h / D 24 h + silymarin group: mild cytoplasmic 8-OHdG expression in spermatocytes (E), IHC-P, bar: 50 µm.
Raw Data for the article: Human Amnion-Derived Mesenchymal Stromal/Stem Cells Pre-Conditioning Inhibits Inflammation and Apoptosis of Immune and Parenchymal Cells in an In Vitro Model of Liver Ischemia/Reperfusion
<p>Ischemia/reperfusion injury (IRI) represents one of the leading causes of primary non-function acute liver transplantation failure. IRI, generated by an interruption of organ blood flow and the subsequent restoration upon transplant, i.e., reperfusion, generates the activation of an inflammatory cascade from the resident Kupffer cells, leading first to neutrophils recruitment and second to apoptosis of the parenchyma. Recently, human mesenchymal stromal/stem cells (hMSCs) and derivatives have been implemented for reducing the damage induced by IRI. Interestingly, sparse data in the literature have described the use of human amnion-derived MSCs (hAMSCs) and, more importantly, no evidence regarding hMSCs priming on liver IRI have been described yet. Thus, our study focused on the definition of an in vitro model of liver IRI to test the effect of primed hAMSCs to reduce IRI damage on immune and hepatic cells. We found that the IFNγ pre-treatment and 3D culture of hAMSCs strongly reduced inflammation induced by M1-differentiated macrophages. Furthermore, primed hAMSCs significantly inhibited parenchymal apoptosis at early timepoints of reperfusion by blocking the activation of caspase 3/7. All together, these data demonstrate that hAMSCs priming significantly overcomes IRI effects in vitro by engaging the possibility of defining the molecular pathways involved in this process.</p>
The Effect of Remote Ischemic Preconditioning on Ischemia/Reperfusion Injury in a Liver Transplant Recipient
ClinicalTrials.gov study NCT03758352. IPD Sharing: UNDECIDED. Countries: 0. Publications: 1.
Melatonin Impact on the Outcomes of Myocardial Ischemia/Reperfusion Injury During Coronary Artery Bypass Grafting Surgery
ClinicalTrials.gov study NCT05552586. IPD Sharing: UNDECIDED. Countries: 0. Publications: 1.
Ischemia/Reperfusion Injury of Human Endothelium: Role of Glucose and Statins
ClinicalTrials.gov study NCT00995670. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Recurrence of Liver Malignancy After Ischemia/Reperfusion Injury
ClinicalTrials.gov study NCT04257240. IPD Sharing: UNDECIDED. Countries: 0. Publications: 10.
Efficacy of Nitric Oxide Administration in Attenuating Ischemia/Reperfusion Injury During Neonatal Cardiopulmonary Bypass
ClinicalTrials.gov study NCT02151877. IPD Sharing: NO. Countries: 1. Publications: 0.
Further inhibition of Histone H2A ubiquitination protects myocardium against ischemia/reperfusion injury through enhancing glycolysis and improving mitochondrial function via promoting Hsp27 expressio
GEO Series GSE225245. Rattus norvegicus. 6 samples. Type: Expression profiling by high throughput sequencing.
ZBP1-mediated apoptosis and inflammation exacerbate steatotic liver ischemia/reperfusion injury
GEO Series GSE254747. Mus musculus. 18 samples. Type: Expression profiling by high throughput sequencing.
RNA-seq analysis of young swine following cardiac ischemia/reperfusion injury.
GEO Series GSE137293. Sus scrofa. 16 samples. Type: Expression profiling by high throughput sequencing.
HO-1 attenuates testicular ischemia/reperfusion injury through activating the phosphorylated c-Jun-miR-221/222-TOX pathway [miRNA]
GEO Series GSE236536. Rattus norvegicus. 6 samples. Type: Non-coding RNA profiling by high throughput sequencing.
Exosomal circEZH2_005, an intestinal injury biomarker, alleviates intestinal ischemia/reperfusion injury by mediating hnRNPA1/Gprc5a signaling
GEO Series GSE227518. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
ATF3 Inhibits Cardiac Ferroptosis by Directly Binding FANCD2 in Response to Myocardial Ischemia/Reperfusion Injury [RNA-Seq 1]
GEO Series GSE193997. Mus musculus. 24 samples. Type: Expression profiling by high throughput sequencing.
Vascular endothelial S1PR2 aggravates cardiac ischemia/reperfusion injury through triggering mitochondrial dysfunctions and endothelial pyroptosis via RHO/ROCK1/DRP1/NLRP3 pathway [heart]
GEO Series GSE245987. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
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