scholarly journals Antioxidant Activity and Cardioprotective Effect of a Nonalcoholic Extract ofVaccinium meridionaleSwartz during Ischemia-Reperfusion in Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Yasmin E. Lopera ◽  
Juliana Fantinelli ◽  
Luisa F. González Arbeláez ◽  
Benjamín Rojano ◽  
José Luis Ríos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Cardiac Tissue ◽  
Ischemia Reperfusion ◽  
Antioxidant Properties ◽  
Thiobarbituric Acid ◽  
Scavenging Activity ◽  
Ischemia And Reperfusion Injury ◽  
Beneficial Effects

Our objective was to assess the antioxidant properties and the effects against the reperfusion injury of a nonalcoholic extract obtained by fermentation from the Colombian blueberry, mortiño (Vaccinium meridionaleSwartz, Ericaceae). Antioxidant properties were assessed byin vitrosystems. To examine the postischemic myocardial function, isolated rat hearts were treated 10 min before ischemia and during the first 10 min of reperfusion with the extract. To analyze the participation of nitric oxide (NO), other experiments were performed in the presence of nitric oxide synthase (NOS) inhibition withNG-nitro-L-arginine methyl ester (L-NAME). In cardiac tissue thiobarbituric acid reactive substances (TBARS) concentration, reduced glutathione (GSH) content, endothelial NOS (eNOS), and Akt expression were also measured. The blueberry extract showed higher total phenols and anthocyanins contents, scavenging activity of superoxide radical and systolic and diastolic function was improved, TBARS diminished, GSH was partially preserved, and both NOS and Akt expression increased in hearts treated with the extract. These beneficial effects were lost when eNOS was inhibited. In resume, these data show that the increase of eNOS expression via Akt and the scavenging activity contribute to the cardioprotection afforded by acute treatment with Colombian blueberry extract against ischemia and reperfusion injury.

Remifentanil Preconditioning Reduces Hepatic Ischemia–Reperfusion Injury in Rats via  Inducible Nitric Oxide Synthase Expression

2011 ◽  
Vol 114 (5) ◽  
pp. 1036-1047 ◽  
Author(s):  
Li-Qun Yang ◽  
Kun-Ming Tao ◽  
Yan-Tao Liu ◽  
Chi-Wai Cheung ◽  
Michael G. Irwin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion ◽  
Inducible Nos

Background Opioid preconditioning against ischemia reperfusion injury has been well studied in myocardial and neuronal tissues. The objective of this study was to determine whether remifentanil could attenuate hepatic injury and to investigate the mechanisms. Methods A rat model of hepatic ischemia reperfusion injury and a hepatocyte hypoxia reoxygenation (HR) injury model were used, respectively, in two series of experiments. Remifentanil was administered before ischemia or hypoxia and the experiments were repeated with previous administration of naloxone, L-arginine and N-ω-nitro-L-arginine methyl ester, a nonselective opioid receptor antagonist, a nitric oxide donor, and nitric oxide synthase (NOS) inhibitor, respectively. Serum aminotransferase, cytokines, and hepatic lipid peroxidation were measured. Histopathology examination and apoptotic cell detection were assessed. For the in vitro study, cell viability, intracellular nitric oxide, apoptosis, and NOS expression were evaluated. Results Remifentanil and L-arginine pretreatment reduced concentrations of serum aminotransferases and cytokines, decreased the concentrations of hepatic malondialdehyde and myeloperoxidase activity, and increased superoxide dismutase, nitric oxide, and inducible NOS expression in vivo. Decreased histologic damage and apoptosis were also seen in these two groups. These changes were prevented by previous administration of N-ω-nitro-L-arginine methyl ester but not naloxone. There was an increase in inducible NOS protein expression but not endogenous NOS in remifentanil and L-arginine pretreated groups compared with control, naloxone, and N-ω-nitro-L-arginine methyl ester groups. Conclusion Pretreatment with remifentanil can attenuate liver injury both in vivo and in vitro. Inducible NOS but not opioid receptors partly mediate this effect by exhausting reactive oxygen species and attenuating the inflammatory response.

scholarly journals Quercetin Liposomal Nanoformulation for Ischemia and Reperfusion Injury Treatment

Pharmaceutics ◽  
2022 ◽  
Vol 14 (1) ◽  
pp. 104
Author(s):  
Margarida Ferreira-Silva ◽  
Catarina Faria-Silva ◽  
Manuela C. Carvalheiro ◽  
Sandra Simões ◽  
Helena Susana Marinho ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Enhanced Recovery ◽  
Antioxidant Properties ◽  
Therapeutic Index ◽  
Drug Carriers ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
Anti Inflammatory

Ischemia and reperfusion injury (IRI) is a common complication caused by inflammation and oxidative stress resulting from liver surgery. Current therapeutic strategies do not present the desirable efficacy, and severe side effects can occur. To overcome these drawbacks, new therapeutic alternatives are necessary. Drug delivery nanosystems have been explored due to their capacity to improve the therapeutic index of conventional drugs. Within nanocarriers, liposomes are one of the most successful, with several formulations currently in the market. As improved therapeutic outcomes have been demonstrated by using liposomes as drug carriers, this nanosystem was used to deliver quercetin, a flavonoid with anti-inflammatory and antioxidant properties, in hepatic IRI treatment. In the present work, a stable quercetin liposomal formulation was developed and characterized. Additionally, an in vitro model of ischemia and reperfusion was developed with a hypoxia chamber, where the anti-inflammatory potential of liposomal quercetin was evaluated, revealing the downregulation of pro-inflammatory markers. The anti-inflammatory effect of quercetin liposomes was also assessed in vivo in a rat model of hepatic IRI, in which a decrease in inflammation markers and enhanced recovery were observed. These results demonstrate that quercetin liposomes may provide a significant tool for addressing the current bottlenecks in hepatic IRI treatment.

scholarly journals A COMPARATIVE STUDY OF IN-VITRO NITRIC OXIDE SCAVENGING ACTIVITY OF BALOFLOXACINVS PRULIFLOXACIN

2016 ◽  
Vol 10 (1) ◽  
pp. 380
Author(s):  
Puja Ranka ◽  
Karthik Vp
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Room Temperature ◽  
Radical Scavenging Activity ◽  
Antioxidant Properties ◽  
Radical Scavenging ◽  
In Vitro Study ◽  
Scavenging Activity ◽  
Acid Reagent

ABSTRACTObjectives: To compare the free radical scavenging activity and antioxidant potentials of balofloxacin versus prulifloxacin.Methods: Nitric oxide (NO) radical scavenging activity was determined using the method of Garret (1964). Sodium nitroprusside in aqueous solutionat physiological pH spontaneously generates NO, which interacts with oxygen to produce nitrite ions which can be determined by the use of Griessilosvay reaction. 2 mm of 10 mm sodium nitroprusside in 0.5 ml phosphate buffer saline (pH 7.4) was mixed with 0.5 ml prulifloxacin and balofloxacinat various concentrations and the mixture incubated at 25°C for 150 minutes. From the incubated mixture 0.5 ml was taken out and added into 1.0 mlsulfanilic acid reagent (30 in 20% glacial acetic acid) and incubated at room temperature for 5 minutes. Finally, 1.0 ml naphthylethylenediaminedihydrochloride (0.1% w/v) was mixed and incubated at room temperature for 30 minutes. The resultant absorbance was recorded at 540 nm using a spectrometer. The percentage inhibition was calculated using the formula:−Abs AbsPercentage inhibition 100control sample= ×AbsResults: At concentration of 10, 20, 30, and 40 µg/ml percentage inhibition observed with prulifloxacin and balofloxacin was 40.94, 53.09, 66.25, 88.06 and 34.49, 49.09, 60.42, and 73.14, respectively. controlConclusion: Thus, this in vitro study suggests that both prulifloxacin and balofloxacin possess antioxidant properties. At the lower doses both thedrugs show similar antioxidant profile, while at the higher doses the antioxidant potential of prulifloxacin is significantly high than balofloxacin.However, the preference of selecting one over the other depends on the indication as well as the risk-benefit ratio.Keywords: In vitro, Nitric oxide, Prulifloxacin, Balofloxacin.

scholarly journals TNFα-Mediated Necroptosis Aggravates Ischemia-Reperfusion Injury in the Fatty Liver by Regulating the Inflammatory Response

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Faji Yang ◽  
Longcheng Shang ◽  
Shuai Wang ◽  
Yang Liu ◽  
Haozhen Ren ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Fatty Liver ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ros Production ◽  
Ischemia And Reperfusion Injury ◽  
Nonalcoholic Fatty Liver ◽  
Neutralizing Monoclonal Antibody

Nonalcoholic fatty liver disease (NAFLD) is more sensitive to ischemia and reperfusion injury (IRI), while there are no effective methods to alleviate IRI. Necroptosis, also known as “programmed necrosis,” incorporates features of necrosis and apoptosis. However, the role of necroptosis in IRI of the fatty liver remains largely unexplored. In the present study, we aimed to assess whether necroptosis was activated in the fatty liver and whether such activation accelerated IRI in the fatty liver. In this study, we found that the liver IRI was enhanced in HFD-fed mice with more release of TNFα. TNFα and supernatant of macrophages could induce necroptosis of hepatocytes in vitro. Necroptosis was activated in NAFLD, leading to more severe IRI, and such necroptosis could be inhibited by TN3-19.12, the neutralizing monoclonal antibody against TNFα. Pretreatment with Nec-1 and GSK′872, two inhibitors of necroptosis, significantly reduced the liver IRI and ROS production in HFD-fed mice. Moreover, the inhibition of necroptosis could decrease ROS production of hepatocytes in vitro. Inflammatory response was activated during IRI, and necroptosis inhibitors could suppress signaling pathways of inflammation and the soakage of inflammation cells. In conclusion, TNFα-induced necroptosis played an important role during IRI in the fatty liver. Our findings demonstrated that necroptosis might be a potential target to reduce the fatty liver-associated IRI.

scholarly journals Ultrasound-Induced Destruction of Nitric Oxide–Loaded Microbubbles in the Treatment of Thrombus and Ischemia–Reperfusion Injury

2022 ◽  
Vol 12 ◽  
Author(s):  
Zenghui Liang ◽  
Huafang Chen ◽  
Xuehao Gong ◽  
Binbin Shi ◽  
Lili Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Acoustic Cavitation ◽  
Liver And Kidney ◽  
Underlying Mechanisms

Objectives: Early recanalization of large vessels in thromboembolism, such as myocardial infarction and ischemic stroke, is associated with improved clinical outcomes. Nitric oxide (NO), a biological gas signaling molecule, has been proven to protect against ischemia–reperfusion injury (IRI). However, the underlying mechanisms remain to be explored. This study investigated whether NO could mitigate IRI and the role of NO during acoustic cavitation.Methods:In vivo, thrombi in the iliac artery of rats were induced by 5% FeCl3. NO-loaded microbubbles (NO-MBs) and ultrasound (US) were used to treat thrombi. B-mode and Doppler US and histological analyses were utilized to evaluate the thrombolysis effect in rats with thrombi. Immunohistochemistry, immunofluorescence, and western blotting were conducted to investigate the underlying mechanisms of NO during acoustic cavitation. In vitro, hypoxia was used to stimulate cells, and NO-MBs were employed to alleviate oxidative stress and apoptosis.Results: We developed NO-MBs that significantly improve the circulation time of NO in vivo, are visible, and effectively release therapeutic gas under US. US-targeted microbubble destruction (UTMD) and NO-loaded UTMD (NO + UTMD) caused a significant decrease in the thrombus area and an increase in the recanalization rates and blood flow velocities compared to the control and US groups. We discovered that UTMD induced NO generation through activation of endothelial NO synthase (eNOS) in vivo. More importantly, we also observed significantly increased NO content and eNOS expression in the NO + UTMD group compared to the UTMD group. NO + UTMD can mitigate oxidative stress and apoptosis in the hind limb muscle without influencing blood pressure or liver and kidney functions. In vitro, NO-MBs alleviated oxidative stress and apoptosis in cells pretreated with hypoxia.Conclusion: Based on these data, UTMD affects the vascular endothelium by activating eNOS, and NO exerts a protective effect against IRI.

scholarly journals Activity of renal organic anion transporters in a model of ischemia and reperfusion injury in vitro

2018 ◽  
pp. 25-27
Author(s):  
V. A. Evteev ◽  
R. E. Kazakov ◽  
A. B. Prokof'ev ◽  
I. A. Mazerkina ◽  
N. D. Bunyatyan
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Organic Anion ◽  
Dicarboxylic Acids ◽  
Organic Anion Transporters ◽  
Ischemia And Reperfusion Injury ◽  
Anion Transporters ◽  
Slc Transporters

The aim of the work is to study the functional characteristics of SLC transporters of organic anions: OAT1 and OAT3 in normal conditions and in model ischemia/reperfusion injury.Materials and methods. The HEK293 cell line was used as a model for the study. Conditions of ischemia/reperfusion injury were created by the previously described method. The activity of the transporters was assessed by the capture of the marker substrate - fluorescein. The concentration of fluorescein was measured using a plate fluorimeter. The results were normalized by the amount of total protein.Results. In condition of ischemia/reperfusion injury, the activity of organic anion transporters decreased in comparison with the norm. The data obtained allow us to conclude that in conditions of ischemia/reperfusion injury, the concentration of dicarboxylic acids in the cell is low, which in turn can lead to a decrease activity of transporters.

scholarly journals Nephroprotective Effects of Polydatin against Ischemia/Reperfusion Injury: A Role for the PI3K/Akt Signal Pathway

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Hong-Bao Liu ◽  
Qiu-Hong Meng ◽  
Chen Huang ◽  
Jian-Bo Wang ◽  
Xiao-Wei Liu
Keyword(s):  
Nitric Oxide ◽  
Molecular Mechanisms ◽  
Glutathione Transferase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Interleukin 1 ◽  
Specific Inhibitor ◽  
Prostaglandin E ◽  
Beneficial Effects

Oxidative stress and inflammation are involved in the pathogenesis in renal ischemia/reperfusion (I/R) injury. It has been demonstrated that polydatin processed the antioxidative, anti-inflammatory, and nephroprotective properties. However, whether it has beneficial effects and the possible mechanisms on renal I/R injury remain unclear. In our present study I/R models were simulated bothin vitroandin vivo. Compared with vehicle control, the administration of polydatin significantly improved the renal function, accelerated the mitogenic response and reduced cell apoptosis in renal I/R injury models, strongly suppressed the I/R-induced upregulation of the expression of tumor necrosis factor-α, interleukin-1β, cyclooxygenase-2, inducible nitric oxide synthase, prostaglandin E-2, and nitric oxide levels, and dramatically decreased contents of malondialdehyde, but it increased the activity of superoxide dismutase, glutathione transferase, glutathione peroxidase and catalase, and the level of glutathione. Further investigation showed that polydatin upregulated the phosphorylation of Akt in kidneys of I/R injury dose-dependently. However, all beneficial effects of polydatin mentioned above were counteracted when we inhibited PI3K/Akt pathway with its specific inhibitor, wortmannin. Taken together, the present findings provide the first evidence demonstrating that PD exhibited prominent nephroprotective effects against renal I/R injury by antioxidative stress and inflammation through PI3-K/Akt-dependent molecular mechanisms.

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