Controlled reperfusion for different durations in the treatment of ischemia–reperfusion injury of the rat ovary: evaluation of biochemical features, molecular gene expression, and histopathology

2015 ◽  
Vol 93 (4) ◽  
pp. 269-274 ◽  
Author(s):  
Omer Erkan Yapca ◽  
Serkan Kumbasar ◽  
Suleyman Salman ◽  
Oguzhan Yarali ◽  
Ebru Sener ◽  
...  
Keyword(s):  
Gene Expression ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Tissue ◽  
Vascular Structures ◽  
Rat Ovary ◽  
Cox 2 ◽  
And Migration ◽  
Controlled Reperfusion

High numbers of proinflammatory cells (PMNLs), which are carried by the blood to ischemic tissue during reperfusion, are considered responsible for inducing the inflammatory response that occurs in ischemia–reperfusion (I/R) injury. Our objective was to determine the controlled reperfusion (CR) interval duration (CRID) that would minimize the injury caused by the PMNLs that infiltrate ischemic tissue. Animal groups were divided into the following groups: Sham group, ovarian I/R group (OIR), and ovarian ischemia controlled-reperfusion groups OICR-1, OICR-2, OICR-3, OICR-4, OICR-5, OICR-6, which had their ovarian artery opened and then closed for 10, 8, 6, 4, 2, or 1 s, respectively. The results show that the COX-2 activity and the gene expression decreased while the COX-1 activity and the gene expression were found to be increased in parallel to the shortening of the period in CRID. From the histopathological examinations, the findings of hemorrhage, edema, congested vascular structures, degenerated cells, and migration and adhesion of PMNLs were scaled as follows: Sham group < OICR-6 < OICR-5 < OICR-4 < OICR-3 < OICR-2 < OICR-1. The results from the histopathological assessments were consistent with the molecular and biochemical findings. In conclusion, our findings suggest that increased COX-2 activity plays a role in I/R injury of the rat ovary, and that controlled reperfusion for 3, 2, or 1 s following 2 h of ischemia may attenuate the effects of I/R injury.

scholarly journals The effect of metamizole on ischemia/reperfusion injury in the rat ovary: An analysis of biochemistry, molecular gene expression, and histopathology

2016 ◽  
Vol 48 (1) ◽  
pp. 32 ◽  
Author(s):  
Bahadir Suleyman ◽  
Serkan Kumbasar ◽  
Suleyman Salman ◽  
RagipAtakan Al ◽  
Cengiz Ozturk ◽  
...  
Keyword(s):  
Gene Expression ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rat Ovary

scholarly journals miR-155 Knockdown Protects against Cerebral Ischemia and Reperfusion Injury by Targeting MafB

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Li Zhang ◽  
Chao Liu ◽  
Chao Huang ◽  
Xiaohui Xu ◽  
Junfang Teng
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Mouse Brain ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Invasion And Migration ◽  
Infarction Volume ◽  
Cox 2 ◽  
And Migration ◽  
Brain Tissues

Background. Studies have elucidated that the variable expression levels of miRNAs influence the inflammatory process in ischemic stroke. Nevertheless, the impact and potential mechanism of miR-155 in cerebral ischemia-reperfusion injury (CIRI) keep to be incompletely known. Methods. The levels of miR-155 and MafB were determined via qRT-PCR, western blot, or immunohistochemistry assays in plasma of patients with CIRI, oxygen glucose deprivation/reoxygenation (OGD/R) induced SH-SY5Y cells, and mouse models with middle cerebral artery occlusion (MCAO). The association between miR-155 and MafB was validated via dual-luciferase reporter and western blot assays. Cell viability, apoptosis, invasion, and migration were evaluated through MTT, flow cytometry, Transwell and wound healing assays. Infarction volume was measured in MCAO mouse brain tissues by TTC assay. The expression of inflammatory mediators was measured by ELISA in cells and brain tissues. Results. miR-155 level was upregulated whereas MafB was downregulated in the plasma of patients with CIRI, OGD/R-induced SH-SY5Y cells, also as mouse models with MCAO injury. Mechanistically, miR-155 directly targeted 3’UTR of MafB and restrained MafB expression in OGD/R injury SH-SY5Y cells. Downregulation of miR-155 attenuated OGD/R-induced injury through increasing proliferation, inhibiting apoptosis, enhancing invasion and migration abilities, and constraining the expression of inflammatory mediators (IL-1β, IL-6, and TNF-α) and inflammatory enzymes (iNOS and COX-2) in SH-SY5Y cells following OGD/R, while MafB inhibition reversed the protective effects. In vivo, downregulating miR-155 reduced the infarction volume in the MACO mouse brain. Furthermore, miR-155 knockdown inhibited the IL-1β, IL-6, TNF-α, iNOS, and COX-2 in the MACO mouse brain tissues. Conclusion. Our results suggest that miR-155 knockdown alleviated ischemia-reperfusion injury by targeting MafB to improve the neurological function and inhibit inflammation response, highlighting a novel therapeutic strategist for CIRI.

scholarly journals The Integrated RNA Landscape of Renal Preconditioning against Ischemia-Reperfusion Injury

2020 ◽  
Vol 31 (4) ◽  
pp. 716-730 ◽  
Author(s):  
Marc Johnsen ◽  
Torsten Kubacki ◽  
Assa Yeroslaviz ◽  
Martin Richard Späth ◽  
Jannis Mörsdorf ◽  
...  
Keyword(s):  
Gene Expression ◽  
Reperfusion Injury ◽  
Caloric Restriction ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hypoxic Preconditioning ◽  
Preventive Strategies ◽  
Gene Expression Signatures

BackgroundAlthough AKI lacks effective therapeutic approaches, preventive strategies using preconditioning protocols, including caloric restriction and hypoxic preconditioning, have been shown to prevent injury in animal models. A better understanding of the molecular mechanisms that underlie the enhanced resistance to AKI conferred by such approaches is needed to facilitate clinical use. We hypothesized that these preconditioning strategies use similar pathways to augment cellular stress resistance.MethodsTo identify genes and pathways shared by caloric restriction and hypoxic preconditioning, we used RNA-sequencing transcriptome profiling to compare the transcriptional response with both modes of preconditioning in mice before and after renal ischemia-reperfusion injury.ResultsThe gene expression signatures induced by both preconditioning strategies involve distinct common genes and pathways that overlap significantly with the transcriptional changes observed after ischemia-reperfusion injury. These changes primarily affect oxidation-reduction processes and have a major effect on mitochondrial processes. We found that 16 of the genes differentially regulated by both modes of preconditioning were strongly correlated with clinical outcome; most of these genes had not previously been directly linked to AKI.ConclusionsThis comparative analysis of the gene expression signatures in preconditioning strategies shows overlapping patterns in caloric restriction and hypoxic preconditioning, pointing toward common molecular mechanisms. Our analysis identified a limited set of target genes not previously known to be associated with AKI; further study of their potential to provide the basis for novel preventive strategies is warranted. To allow for optimal interactive usability of the data by the kidney research community, we provide an online interface for user-defined interrogation of the gene expression datasets (http://shiny.cecad.uni-koeln.de:3838/IRaP/).

scholarly journals Effects of Apigenin on Experimental Ischemia/Reperfusion Injury in the Rat Ovary

2017 ◽  
Vol 34 (5) ◽  
pp. 444-449 ◽  
Author(s):  
Zeynep Soyman ◽  
Sefa Kelekçi ◽  
Veysel Sal ◽  
Osman Şevket ◽  
Nihan Bayındır ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rat Ovary

Cardiac specific overexpression of COX-2 protects against ischemia/reperfusion injury

2007 ◽  
Vol 42 (6) ◽  
pp. S200
Author(s):  
Javier Inserte ◽  
Belen Molla ◽  
Victor Hernando ◽  
Paloma Martín-Sanz ◽  
Lisardo Boscá ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cox 2

Dexmedetomidine Suppressing Apoptosis to Release Rats’ Liver Ischemia-Reperfusion Injury

2021 ◽  
Vol 11 (8) ◽  
pp. 1536-1542
Author(s):  
Zhao Hai-Fan ◽  
Li Chong ◽  
Hu Zhi-Duo ◽  
Chen Hong ◽  
Jiang Tao ◽  
...  
Keyword(s):  
Western Blot ◽  
Liver Tissue ◽  
Caspase 3 ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Pathological State ◽  
Inhibitory Effects ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

Purpose: Explore the dexmedetomidine’s therapeutic impact on hepatic ischemia-reperfusion (I/R) injury and the related principle. Methods: The work established the rats’ liver I/R model. Liver tissues’ pathological state from each rat was evaluated by HE staining. ELISA was utilized to confirm the activity of MDA and SOD in the liver tissue, AST in the serum, and the ALT’s concentration. The apoptotic state of liver tissue was detected by TUNEL assay. Bcl-2, Caspase-3, HO-1, and BAX’s expressions of each rat’s liver tissue had been confirmed through immunohistochemistry and western blot. Results: Rats’ liver injury from I/R group and DEX+A group was rat’s liver tissue had been confirmed through immunohistochemistry and western blot. severer than that from Sham group in terms of HE staining and ELISA. The injured tissue has been improved by the introduction of Dexmedetomidine. The TUNEL, Immunohistochemistry and Western Blot results indicated that the high apoptotic rate in I/R model was inhibited using Dexmedetomidine. However, the inhibitory effects were reversed by the co-administration of Atipamezole. Conclusion: Dexmedetomidine suppressed apoptosis to alleviate rats’ hepatic ischemia-reperfusion injuries.

scholarly journals STUDY ON THE SYNTHESIS OF PUERARIN DERIVATIVES AND THEIR ANTI-VASCULAR DEMENTIA ACTIVITY

2016 ◽  
Vol 8 (2) ◽  
pp. 11
Author(s):  
Pei Jiang
Keyword(s):  
Vascular Dementia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cyclooxygenase 2 ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
H Nmr ◽  
Cox 2 ◽  
Oxide Synthase

<p class="lead">In this study, puerarin derivatives were designed by adding an active acetonitrile group that inhibits cyclooxygenase-2 (COX-2) in order to enhance the anti-vascular dementia drug activity. The acetonitrile group was linked to puerarin at the 7/4 'positions by a phenolic hydroxyl to give 7-mono-and 7, 4' di-substituted derivatives of puerarin. These structures were confirmed by <sup>1</sup>H NMR spectroscopy and MS spectroscopy. We compared the affinity of puerarin derivatives and puerarin for cyclooxygenase-2 (COX-2) using molecular docking. In addition, the anti-vascular dementia activity of the developed puerarin derivatives was studied by water maze, novel object recognition, and the determination of inducible nitric oxide synthase (iNOS) enzyme activity at the cerebral cortex of mice. Experimental results showed that the puerarin derivatives have a good affinity for COX-2 with therapeutic effects against vascular dementia. The results of this study suggest that the protective effects of the puerarin derivatives against vascular dementia may be related to suppression of inflammation associated with ischemia-reperfusion injury through inhibition of COX-2.</p>

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