Inhalation of hydrogen gas suppresses hepatic injury caused by ischemia/reperfusion through reducing oxidative stress

The purpose of this study was to investigate the protective effects of hydrogen reducing ischemia-reperfusion injury during CO2 pneumoperitoneum on oxidative stress and liver function. Eighteen healthy Beagle dogs were divided into three groups. Dogs in the control group were subjected only to anesthesia for 90 min. The pneumoperitoneum group was subjected to the pressure of CO2 pneumoperitoneum with 12 mmHg intraabdominal pressure for 90 min. The hydrogen group was subjected to the pressure of CO2 pneumoperitoneum with 12 mmHg intra-abdominal pressure for 90 min after a subcutaneous injection of hydrogen gas (0.2 mL/kg) for 10 min. Blood samples were collected before the induction of pneumoperitoneum, as well as 2 h and 6 h after deflation, to evaluate oxidative stress and liver function in serum. Liver tissue samples were taken 6 h after deflation for histopathological examination. In comparison with group P, a milder histopathological change was found in group H2, and the levels of hepatic function and anti-oxidation in group H2 were higher. Hydrogen gas reduced liver ischemia-reperfusion injury due to CO2 pneumoperitoneum by reducing oxidative stress and improving liver function. Hydrogen gas therapy can be considered as a way to reduce liver ischemiareperfusion injury in laparoscopic surgery.

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Spironolactone Effect in Hepatic Ischemia/Reperfusion Injury in Wistar Rats

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/3196431 ◽

2016 ◽

Vol 2016 ◽

pp. 1-9 ◽

Cited By ~ 2

Author(s):

Julio César Jiménez Pérez ◽

Araní Casillas Ramírez ◽

Liliana Torres González ◽

Linda Elsa Muñoz Espinosa ◽

Marlene Marisol Perales Quintana ◽

...

Keyword(s):

Oxidative Stress ◽

Catalase Activity ◽

Hepatic Injury ◽

Cytokine Production ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Apoptotic Bodies ◽

Hepatic Ischemia ◽

Hepatic Ischemia Reperfusion ◽

And Oxidative Stress

Introduction. Ischemia/reperfusion (IR) injury, often associated with liver surgery, is an unresolved problem in the clinical practice. Spironolactone is an antagonist of aldosterone that has shown benefits over IR injury in several tissues, but its effects in hepatic IR are unknown.Objective. To evaluate the effect of spironolactone on IR-induced damage in liver.Materials and Methods. Total hepatic ischemia was induced in rats for 20 min followed by 60 min of reperfusion. Spironolactone was administered and hepatic injury, cytokine production, and oxidative stress were assessed.Results. After IR, increased transaminases levels and widespread acute inflammatory infiltrate, disorganization of hepatic hemorrhage trabeculae, and presence of apoptotic bodies were observed. Administration of SPI reduced biochemical and histological parameters of liver injury. SPI treatment increased IL-6 levels when compared with IR group but did not modify either IL-1βor TNF-αwith respect to IR group. Regarding oxidative stress, increased levels of catalase activity were recorded in IR + SPI group in comparison with group without treatment, whereas MDA levels were similar in IR + SPI and IR groups.Conclusions. Spironolactone reduced the liver damage induced by IR, and this was associated with an increase in IL-6 production and catalase activity.

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Effects of Off-Pump Versus On-Pump Coronary Artery Bypass Grafting: Apoptosis, Inflammation, and Oxidative Stress

The Heart Surgery Forum ◽

10.1532/hsf98.2014326 ◽

2014 ◽

Vol 17 (5) ◽

pp. 271 ◽

Cited By ~ 7

Author(s):

Murat Bicer ◽

Tunay Senturk ◽

Murat Yanar ◽

Ahmet Tutuncu ◽

Arzu Yilmaztepe Oral ◽

...

Keyword(s):

Oxidative Stress ◽

Ischemia Reperfusion ◽

Artery Bypass ◽

Bypass Grafting ◽

Artery Bypass Grafting ◽

Cabg Surgery ◽

Off Pump ◽

Pump Cabg ◽

Hs Crp ◽

And Oxidative Stress

Background: It has been suggested that off-pump coronary artery bypass grafting (CABG) surgery reduces myocardial ischemia-reperfusion injury, postoperative systemic inflammatory response, and oxidative stress. The aim of this study was to measure serum malondialdehyde (MDA), highsensitivity C-reactive protein (hs-CRP), M30, and M65 levels and to investigate the relationship between M30 levels and oxidative stress and inflammation in patients undergoing onand off-pump CABG surgery. Methods: Fifty patients were randomly assigned to onpump or off-pump CABG surgery (25 patients off-pump and 25 on-pump CABG surgery), and blood samples were collected prior to surgery, and 30 minutes, 60 minutes, 6 hours, and 24 hours after CABG surgery. Results: Compared to the on-pump group, serum MDA levels at 30 minutes, 60 minutes, 6 hours, and 24 hours after the CABG surgery were significantly lower in the off-pump group (P = .001, P = .001, P = .001, and P = .001, respectively). Serum M30 levels were found to be elevated in both groups, returning to baseline at 24 hours. When compared to baseline, the hs-CRP level reached its peak at 24 hours at 13.28 ± 5.32 mg/dL in the on-pump group, and 15.44 ± 4.02 mg/dL in the off-pump group. Conclusion: CABG surgery is associated with an increase in inflammatory markers and serum M30 levels, indicating epithelial/endothelial apoptosis in the early period.

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Effects of Genipin at NO synthesis and Ischemia-Reperfusion Induced Oxidative Stress in Old Rat Hearts

International Journal of Physiology and Pathophysiology ◽

10.1615/intjphyspathophys.v1.i4.40 ◽

2010 ◽

Vol 1 (4) ◽

pp. 335-344 ◽

Cited By ~ 1

Author(s):

Yulia V. Goshovska ◽

Yulia P. Korkach ◽

Tatiana V. Shimanskaya ◽

Anatolii V. Kotsuruba ◽

Vadym F. Sagach

Keyword(s):

Oxidative Stress ◽

Ischemia Reperfusion ◽

Rat Hearts

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Evaluation of the Timing of Administration of Edaravone on Its Protection against Acetaminophen-Induced Hepatic Injury and Oxidative Stress in the Rat

10.26226/morressier.57d6b2bfd462b8028d88edcc ◽

2016 ◽

Author(s):

Cesar Lau-Cam

Keyword(s):

Oxidative Stress ◽

Hepatic Injury ◽

And Oxidative Stress

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Danshensu Rescues Ischemia/Reperfusion Caused Human Hepatocyte Death

Current Topics in Nutraceutical Research ◽

10.37290/ctnr2641-452x.17:117-121 ◽

2018 ◽

Vol 17 (2) ◽

pp. 117-121

Author(s):

Sun Maw-Sheng ◽

Liang Chun-Ya ◽

Hsieh Po-Chun ◽

Kuo Chan-Yen

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Caspase 3 ◽

Ischemia Reperfusion ◽

Oxygen Species ◽

Good Strategy ◽

Ros Accumulation ◽

Dichlorofluorescin Diacetate ◽

Hepatocyte Damage ◽

Hepatocyte Death

Apoptosis of hepatocyte, under ischemia/reperfusion (IR) conditions, has been identified as an essential process in the progression of liver transplantation. Under these conditions, mitochondria can become a threat to the cell because of their capacity to generate reactive oxygen species (ROS). Additionally, ROS overproduction may induce inflammation. As ROS accumulation appears to cause hepatocyte damage or death, there has been considerable interest in identifying the candidate natural products involved and in developing strategies to reduce oxidative stress. In this study, we use Danshensu as a candidate product to speculate whether has the protective effect on apoptotic hepatocyte upon IR. To speculate the apoptotic phenomena was reversed by Danshensu, we detected the p53, cleaved-caspase 3 expression by western blotting, as well as caspase-3 activity. Additionally, we analyzed the ROS levels by 2′,7′-dichlorofluorescin diacetate (DCF-DA) staining. We also detected the cell viability by WST-1. Results showed that Danshensu alleviated hypoxia-caused cell apoptosis via ROS overproduction. We suggested that Danshensu is a good strategy for treating hepatocyte damage upon IR.

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Molecular Dissection of Renal Ischemia-Reperfusion: Oxidative Stress and Cellular Events

Current Medicinal Chemistry ◽

10.2174/0929867323666160112122858 ◽

2016 ◽

Vol 23 (19) ◽

pp. 1965-1980 ◽

Cited By ~ 27

Author(s):

Branislav Rovcanin ◽

Branislava Medic ◽

Gordana Kocic ◽

Tatjana Cebovic ◽

Marko Ristic ◽

...

Keyword(s):

Oxidative Stress ◽

Ischemia Reperfusion ◽

Renal Ischemia ◽

Molecular Dissection ◽

Cellular Events

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LncRNA SNHG12 Improves Cerebral Ischemic-reperfusion Injury by Activating SIRT1/FOXO3a Pathway through I nhibition of Autophagy and Oxidative Stress

Current Neurovascular Research ◽

10.2174/1567202617666200727142019 ◽

2020 ◽

Vol 17 (4) ◽

pp. 394-401

Author(s):

Yuanhua Wu ◽

Yuan Huang ◽

Jing Cai ◽

Donglan Zhang ◽

Shixi Liu ◽

...

Keyword(s):

Oxidative Stress ◽

Molecular Mechanisms ◽

Ischemia Reperfusion ◽

Critical Role ◽

Cell Activity ◽

Ht22 Cells ◽

Cerebral Ischemic ◽

Cerebral Ischemic Reperfusion ◽

And Oxidative Stress

Background: Ischemia/reperfusion (I/R) injury involves complex biological processes and molecular mechanisms such as autophagy. Oxidative stress plays a critical role in the pathogenesis of I/R injury. LncRNAs are the regulatory factor of cerebral I/R injury. Methods: This study constructs cerebral I/R model to investigate role of autophagy and oxidative stress in cerebral I/R injury and the underline regulatory mechanism of SIRT1/ FOXO3a pathway. In this study, lncRNA SNHG12 and FOXO3a expression was up-regulated and SIRT1 expression was down-regulated in HT22 cells of I/R model. Results: Overexpression of lncRNA SNHG12 significantly increased the cell viability and inhibited cerebral ischemicreperfusion injury induced by I/Rthrough inhibition of autophagy. In addition, the transfected p-SIRT1 significantly suppressed the release of LDH and SOD compared with cells co-transfected with SIRT1 and FOXO3a group and cells induced by I/R and transfected with p-SNHG12 group and overexpression of cells co-transfected with SIRT1 and FOXO3 further decreased the I/R induced release of ROS and MDA. Conclusion: In conclusion, lncRNA SNHG12 increased cell activity and inhibited oxidative stress through inhibition of SIRT1/FOXO3a signaling-mediated autophagy in HT22 cells of I/R model. This study might provide new potential therapeutic targets for further investigating the mechanisms in cerebral I/R injury and provide.

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MiR-485-5p Promotes Neuron Survival through Mediating Rac1/Notch2 Signaling Pathway after Cerebral Ischemia/Reperfusion

Current Neurovascular Research ◽

10.2174/1567202617666200415154822 ◽

2020 ◽

Vol 17 (3) ◽

pp. 259-266 ◽

Cited By ~ 2

Author(s):

Xuan Chen ◽

Sumei Zhang ◽

Peipei Shi ◽

Yangli Su ◽

Dong Zhang ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Viability ◽

Therapeutic Option ◽

Ischemia Reperfusion ◽

Glucose Deprivation ◽

Small Gtpase ◽

Luciferase Reporter ◽

Pathological Feature ◽

In Cells

Objective: Ischemia-reperfusion (I/R) injury is a pathological feature of ischemic stroke. This study investigated the regulatory role of miR-485-5p in I/R injury. Methods: SH-SY5Y cells were induced with oxygen and glucose deprivation/reoxygenation (OGD/R) to mimic I/R injury in vitro. Cells were transfected with designated constructs (miR-485- 5p mimics, miR-485-5p inhibitor, lentiviral vectors overexpressing Rac1 or their corresponding controls). Cell viability was evaluated using the MTT assay. The concentrations of lactate dehydrogenase, malondialdehyde, and reactive oxygen species were detected to indicate the degree of oxidative stress. Flow cytometry and caspase-3 activity assay were used for apoptosis assessment. Dual-luciferase reporter assay was performed to confirm that Rac family small GTPase 1 (Rac1) was a downstream gene of miR-485-5p. Results: OGD/R resulted in decreased cell viability, elevated oxidative stress, increased apoptosis, and downregulated miR-485-5p expression in SH-SY5Y cells. MiR-485-5p upregulation alleviated I/R injury, evidenced by improved cell viability, decreased oxidative markers, and reduced apoptotic rate. OGD/R increased the levels of Rac1 and neurogenic locus notch homolog protein 2 (Notch2) signaling-related proteins in cells with normal miR-485-5p expression, whereas miR- 485-5p overexpression successfully suppressed OGD/R-induced upregulation of these proteins. Furthermore, the delivery of vectors overexpressing Rac1 in miR-485-5p mimics-transfected cells reversed the protective effect of miR-485-5p in cells with OGD/R-induced injury. Conclusion: This study showed that miR-485-5p protected cells following I/R injury via targeting Rac1/Notch2 signaling suggest that targeted upregulation of miR-485-5p might be a promising therapeutic option for the protection against I/R injury.

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