Plasma obtained following murine hindlimb ischemic conditioning protects against oxidative stress in zebrafish models through activation of nrf2a and downregulation of duox

Ischemia/reperfusion of organ systems in trauma patients with resuscitated hemorrhagic shock (HSR) contributes to tissue injury and organ dysfunction. Previous studies using a murine model of HSR showed that remote ischemic preconditioning (RIC) protected against organ injury and that the plasma was able to prevent neutrophil migration in a zebrafish tailfin-cut inflammation model. In this study, we hypothesized that RIC plasma inhibits neutrophil function through a decrease in reactive oxygen species (ROS) production via the upregulation of the transcription factor Nrf2 and downstream antioxidative genes. Plasma from mice subjected to RIC (4 cycles of 5-min hindlimb ischemia/reperfusion) was microinjected into zebrafish. The results show that RIC plasma caused a reduction of ROS generation in response to tail injury. In addition, RIC plasma protected the fish larvae in the survival studies when exposed to either H2O2 or LPS. Oxidative stress PCR Array showed that RIC plasma treatment led to upregulation of antioxidative related genes including hsp70, hmox1a, nqo1 as well as downregulation of duox, the producer of H2O2. To explore the role of nrf2 in RIC, RIC plasma from Nrf2 KO mice were injected to the zebrafish and showed no inhibitory effect on neutrophil migration. Moreover, knockdown of nrf2a attenuated the anti-inflammatory and protective effect of RIC plasma. The downregulation of duox and upregulation of hmox1a were confirmed to require the activation of nrf2a. Therefore, we show that the protective effect of RIC may be related to the elaboration of humoral factors which counter injury-induced ROS generation in a nrf2-dependent fashion.

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miR-187 Modulates Cardiomyocyte Apoptosis and Oxidative Stress in Myocardial Infarction Mice via Negatively Regulating DYRK2

10.21203/rs.3.rs-291355/v1 ◽

2021 ◽

Author(s):

Fen Zhu ◽

Zhili Yu ◽

Dongsheng Li

Keyword(s):

Oxidative Stress ◽

Myocardial Infarction ◽

Protective Effect ◽

Ischemia Reperfusion ◽

Annexin V ◽

Cardiomyocyte Apoptosis ◽

Ros Generation ◽

And Oxidative Stress

Abstract Background: Myocardial infarction is a serious representation of cardiovescular disease, however, ischemia–reperfusion (I/R) injury is an unpredictable complication of cardiovascular surgeries.Methods: MiR-187 or DYRK2 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with miR-187 mimic or inhibitor or DYRK2 inhibitor to confirm the function of miR-187 in H/R. A myocardium I/R mouse model was established using miR-187 transgenic mice. Circulating levels of miR-187 or DYRK2 was detected by quantitative realtime PCR and protein expression was detected by western blotting. The cell viability in all groups was determined by MTT assay and the apoptosis ratio was detected by flow cytometry after staining with Annexin V-FITC. The effect of miR-187 on cellular ROS generation was examined by DCFH-DA. The level of lipid peroxidation and SOD expression were determined by MDA and SOD assay. Results: The findings indicated that miR-187 may be a possible regulator in the protective effect of H/R-induced cardiomyocyte apoptosis, cellular oxidative stress and leaded to DYRK2 suppression at a posttranscriptional level. Moreover, the improvement of miR-187 on H/R-induced cardiomyocyte injury contributed to the obstruction of DYRK2 expression. In addition, these results identified DYRK2 as the functional downstream target of miR-187 regulated myocardial infarction and oxidative stress. Conclusions: These present work provided the first insight into the function of miR-187 in successfully protect cardiomyocyte both in vivo and in vitro, and such a protective effect were mediated through the regulation of DYRK2 expression. Trial registration: Not Applicable.

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The possible protective effect of colchicine against liver damage induced by renal ischemia–reperfusion injury: role of Nrf2 and NLRP3 inflammasome

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2020-0230 ◽

2020 ◽

Vol 98 (12) ◽

pp. 849-854

Author(s):

Azza Sayed Awad ◽

Hemat A. Elariny ◽

Amany Said Sallam

Keyword(s):

Oxidative Stress ◽

Liver Injury ◽

Protective Effect ◽

Reperfusion Injury ◽

Nlrp3 Inflammasome ◽

Inflammatory Responses ◽

Ischemia Reperfusion Injury ◽

Tissue Injury ◽

Ischemia Reperfusion ◽

Sham Operation

Ischemia–reperfusion injury (IRI) induces an inflammatory response and production of reactive oxygen species, which affects the organs remote to the sites of renal IR. However, remote effects of renal IRI on the liver need further investigations. Renal injury associated with liver disease is a common clinical problem. Colchicine is an established drug for microtubule stabilization that may reduce tissue injury and has antioxidant and antiinflammatory effects. The aim of the present study was (i) to assess the hepatic changes after induction of renal IRI, (ii) to explore the possible protective effect of colchicine on liver injury following renal IRI, and (iii) to investigate the possible mechanisms underlying the potential effect. Forty rats were randomly divided into four groups: sham operation group, colchicine-treated group, IR group, and colchicine-treated IR group. Colchicine treatment improved liver function (ALT/AST) after renal IRI, decreased hepatic oxidative stress and cell apoptosis by reducing hepatic MDA, upregulating hepatic total antioxidant capacity, Nrf2, and HO-1. Furthermore, colchicine inhibited inflammatory responses by downregulating hepatic NLRP3 inflammasome, IL-1β, and caspase-1. Colchicine attenuates renal IRI-induced liver injury in rats. This effect may be due to reducing inflammation and oxidative stress markers.

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Prostaglandin-E 1 has a protective effect on renal ischemia/reperfusion-induced oxidative stress and inflammation mediated gastric damage in rats

International Immunopharmacology ◽

10.1016/j.intimp.2016.04.021 ◽

2016 ◽

Vol 36 ◽

pp. 142-150 ◽

Cited By ~ 12

Author(s):

Selda Gezginci-Oktayoglu ◽

Nurcan Orhan ◽

Sehnaz Bolkent

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

Ischemia Reperfusion ◽

Renal Ischemia ◽

Gastric Damage ◽

Prostaglandin E

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miR-187 modulates cardiomyocyte apoptosis and oxidative stress in myocardial infarction mice via negatively regulating DYRK2

10.22514/sv.2021.137 ◽

2021 ◽

Keyword(s):

Oxidative Stress ◽

Myocardial Infarction ◽

Protective Effect ◽

Myocardial Infarct ◽

Annexin V ◽

Cardiomyocyte Apoptosis ◽

Ros Generation ◽

Downstream Target

Myocardial infarction is a serious representation of cardiovescular disease, MicroRNAs play a role in modifying I/R injury and myocardial infarct remodeling. The present study therefore examined the potential role of miR-187 in cardiac I/R injury and its underlying mechanisms. miR-187 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with miR-187 mimic or inhibitor to confirm the function of miR-187 in H/R. DYRK2 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with DYRK2 inhibitor. A myocardium I/R mouse model was established. Circulating levels of miR-187 or DYRK2 was detected by quantitative realtime PCR and protein expression was detected by western blotting. The cell viability in all groups was determined by MTT assay and the apoptosis ratio was detected by flow cytometry after staining with Annexin V-FITC. The effect of miR-187 on cellular ROS generation was examined by DCFH-DA. The level of lipid peroxidation and SOD expression were determined by MDA and SOD assay. The findings indicated that miR-187 may be a possible regulator in the protective effect of H/R-induced cardiomyocyte apoptosis, cellular oxidative stress and leaded to DYRK2 suppression at a posttranscriptional level. Moreover, the improvement of miR-187 on H/R-induced cardiomyocyte injury contributed to the obstruction of DYRK2 expression. In addition, these results identified DYRK2 as the functional downstream target of miR-187 regulated myocardial infarction and oxidative stress.These present work provided the first insight into the function of miR-187 in successfully protect cardiomyocyte both in vivo and in vitro, and such a protective effect were mediated through the regulation of DYRK2 expression.

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Protective effect of CTRP6 on cerebral ischemia/reperfusion injury by attenuating inflammation, oxidative stress and apoptosis in PC12 cells

Molecular Medicine Reports ◽

10.3892/mmr.2020.11108 ◽

2020 ◽

Vol 22 (1) ◽

pp. 344-352

Author(s):

Ying Li ◽

Jie Sun ◽

Lei Gu ◽

Xufang Gao

Keyword(s):

Oxidative Stress ◽

Cerebral Ischemia ◽

Protective Effect ◽

Reperfusion Injury ◽

Pc12 Cells ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Cerebral Ischemia Reperfusion ◽

Cerebral Ischemia Reperfusion Injury

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Corrigendum to “Protective effect of dioscin against intestinal ischemia/reperfusion injury via adjusting miR-351-5p-mediated oxidative stress” [Pharmacol. Res. 137 (2018) 56–63]

Pharmacological Research ◽

10.1016/j.phrs.2019.104322 ◽

2019 ◽

Vol 146 ◽

pp. 104322

Author(s):

Yupeng Hu ◽

Zhang Mao ◽

Lina Xu ◽

Lianhong Yin ◽

Xufeng Tao ◽

...

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

Reperfusion Injury ◽

Intestinal Ischemia ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Intestinal Ischemia Reperfusion

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Safflor Yellow B Attenuates Ischemic Brain Injury via Downregulation of Long Noncoding AK046177 and Inhibition of MicroRNA-134 Expression in Rats

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/4586839 ◽

2020 ◽

Vol 2020 ◽

pp. 1-20

Author(s):

Chaoyun Wang ◽

Hongzhi Wan ◽

Qiaoyun Wang ◽

Hongliu Sun ◽

Yeying Sun ◽

...

Keyword(s):

Oxidative Stress ◽

Brain Injury ◽

Ischemia Reperfusion ◽

Cell Activity ◽

Neuronal Injury ◽

The Body ◽

Ros Generation ◽

Related Factor ◽

Cell Respiration ◽

Oxidative Balance

Stroke breaks the oxidative balance in the body and causes extra reactive oxygen species (ROS) generation, leading to oxidative stress damage. Long noncoding RNAs (lncRNAs) and microRNAs play pivotal roles in oxidative stress-mediated brain injury. Safflor yellow B (SYB) was able to effectively reduce ischemia-mediated brain damage by increasing antioxidant capacity and inhibiting cell apoptosis. In this study, we investigated the putative involvement of lncRNA AK046177 and microRNA-134 (miR-134) regulation in SYB against ischemia/reperfusion- (I/R-) induced neuronal injury. I/R and oxygen-glucose deprivation/reoxygenation (OGD/R) were established in vivo and in vitro. Cerebral infarct volume, neuronal apoptosis, and protein expression were detected. The effects of SYB on cell activity, cell respiration, nuclear factor erythroid 2-related factor 2 (Nrf2), antioxidant enzymes, and ROS were evaluated. I/R or OGD/R upregulated the expression of AK046177 and miR-134 and subsequently inhibited the activation and expression of CREB, which caused ROS generation and brain/cell injury. SYB attenuated the effects of AK046177, inhibited miR-134 expression, and promoted CREB activation, which in turn promoted Nrf2 expression, and then increased antioxidant capacities, improved cell respiration, and reduced apoptosis. We suggested that the antioxidant effects of SYB were driven by an AK046177/miR-134/CREB-dependent mechanism that inhibited this pathway, and that SYB has potential use in reducing or possibly preventing I/R-induced neuronal injury.

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Protective Effect of the Total Flavonoids from Rosa laevigata Michx Fruit on Renal Ischemia-Reperfusion Injury through Suppression of Oxidative Stress and Inflammation

Molecules ◽

10.3390/molecules21070952 ◽

2016 ◽

Vol 21 (7) ◽

pp. 952 ◽

Cited By ~ 27

Author(s):

Lisha Zhao ◽

Lina Xu ◽

Xufeng Tao ◽

Xu Han ◽

Lianhong Yin ◽

...

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Renal Ischemia ◽

Total Flavonoids ◽

Renal Ischemia Reperfusion Injury ◽

Rosa Laevigata

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Protective effect of chlorogenic acid on renal ischemia/reperfusion injury in rats

Archivio Italiano di Urologia e Andrologia ◽

10.4081/aiua.2020.2.153 ◽

2020 ◽

Vol 92 (2) ◽

Author(s):

Tuncay Toprak ◽

Cagri Akin Sekerci ◽

Hasan Riza Aydın ◽

Mehmet Akif Ramazanoglu ◽

Fatma Demet Arslan ◽

...

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

Chlorogenic Acid ◽

Tissue Damage ◽

Sham Group ◽

Ischemia Reperfusion ◽

Statistical Significance ◽

Histological Evaluation ◽

Renal Histology ◽

Biochemical Examination

Objectives: Ischemia/reperfusion (I/R) injury is a common cause of renal injury and to date, many pharmacological agents have been identified to decrease I/R injury. One of the potential compound that can target I/R injury is chlorogenic acid (CGA). It has potent antiinflammatory, antibacterial, anti-oxidant, analgesic and antipyretic activities in in vitro experiments and in vivo animal models. The aim of the study was to investigate the protective characteristic of CGA on renal I/R injury. Material and Methods: 24 rats were randomly allocated to three groups (n = 8): Sham, I/R+CGA and I/R groups. CGA was administered intraperitoneally at a dose of 20 mg/kg, 10 min before reperfusion. I/R injury was achieved by clamping the left renal artery for 45 minutes, followed by reperfusion for 4 hours. The left kidneys of the rats were examined for tissue damage by histopathological and biochemical examination. For histological evaluation, EGTI scoring system was used. For biochemical examination total oxidant status, total antioxidant status and oxidative stress index were used. The power analysis indicated that 8 subjects per group would be required to produce 80% chance of achieving statistical significance at p < 0.05 level. The results are expressed as mean ± SD. Mann- Whitney U was performed for statistical analysis. Results: Histopathological examination of the tissue damage revealed that all kidneys in the sham group were normal. I-R group had significantly higher histopathological scores than other groups. Histopathological improvement was seen after CGA treatment. TAS, TOS and OSI values of I-R group were significantly higher than sham group (0.88 vs 0.76 (p: 0.004), 13.8 vs 7.04 (p: 0.021) and 0.15 vs 0.09 (p: 0.034), respectively). In CGA treated group TAS, TOS and OSI levels were 0.84, 6.47 and 0.07, respectively. CGA treatment resulted in significant improvement in TOS and OSI parameters. Conclusions: CGA treatment provided marked improvement in renal histology and suppressed oxidative stress. Thus, CGA may have a protective effect in renal tissue against I/R injury.

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