Niacin Ameliorates Kidney Warm Ischemia and Reperfusion Injury–Induced Ventricular Dysfunction and Oxidative Stress and Disturbance in Mitochondrial Metabolism in Rats

Tai, Sichao; Fu, Yao; Yang, Yongyao; Wang, J.J.

doi:10.1016/j.transproceed.2014.11.057

Cited by 12 publications

(5 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the clinical peri-operative period, I/R injury occurs quite frequently, producing redundant ROS, leading to a multi-organ oxidative stress, including that in the kidneys ( 34 ). It has been shown that in rat renal I/R injury, the disrusption of mitochondrial metabolism and oxidative stress, results in ventricular function disorder, and leads to cardiac and renal injury ( 35 ). High glucose levels have been shown to highly associated with a a lower tolerance to ischemia, and an increased severity of renal I/R injury ( 36 , 37 ).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of DJ-1 reduces oxidative stress and attenuates hypoxia/reoxygenation injury in NRK-52E cells exposed to high glucose

Shen

Sun

Xia

et al. 2016

International Journal of Molecular Medicine

View full text Add to dashboard Cite

Patients with diabetes are more vulnerable to renal ischemia/reperfusion (I/R) injury, which is implicated in hyperglycemia-induced oxidative stress. We previously reported that the hyperglycemia-induced inhibition of DJ-1, a novel oncogene that exhibits potent antioxidant activity, is implicated in the severity of myocardial I/R injury. In the present study, we aimed to explore the role of DJ-1 in hypoxia/reoxygenation (H/R) injury in renal cells exposed to high glucose (HG). For this purpose, NRK-52E cells were exposed to HG (30 mM) for 48 h and then exposed to hypoxia for 4 h and reoxygenation for 2 h, which significantly decreased cell viability and superoxide dismutase (SOD) activity, and increased the malondialdehyde (MDA) content, accompanied by a decrease in DJ-1 protein expression. The overexpression of DJ-1 by transfection with a DJ-1 overexpression plasmid exerted protective effects against HG-induced H/R injury, as evidenced by increased CCK-8 levels and SOD activity, the decreased release of lactate dehydrogenase (LDH) and the decreased MDA content, and increased nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and heme oxygenase-1 (HO-1) expression. Similar effects were observed following treatment with the antioxidant, N-acetylcysteine. These results suggest that the overexpression of DJ-1 reduces oxidative stress and attenuates H/R injury in NRK-52E cells exposed to HG.

show abstract

Section: Discussionmentioning

confidence: 99%

Overexpression of DJ-1 reduces oxidative stress and attenuates hypoxia/reoxygenation injury in NRK-52E cells exposed to high glucose

Shen

Sun

Xia

et al. 2016

International Journal of Molecular Medicine

View full text Add to dashboard Cite

show abstract

“…A randomized controlled clinical trial reported that niacin improves both 6- and 15-year mortality of patients after myocardial infarction with or without metabolic syndrome thereby suggesting a cardioprotective effect for niacin [ 88 ]. Direct cardioprotective effect of niacin was reported in preclinical studies as well [ 89 – 92 ]. However, evidence is not available to clarify the potential beneficial effect of niacin in cholesterol-induced cardiac stress.…”

Section: Modulation Of Hypercholesterolemia-induced Oxidative/nitrmentioning

confidence: 99%

Modulation of Hypercholesterolemia‐Induced Oxidative/Nitrative Stress in the Heart

Csonka

Sárközy

Pipicz

et al. 2015

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Hypercholesterolemia is a frequent metabolic disorder associated with increased risk for cardiovascular morbidity and mortality. In addition to its well-known proatherogenic effect, hypercholesterolemia may exert direct effects on the myocardium resulting in contractile dysfunction, aggravated ischemia/reperfusion injury, and diminished stress adaptation. Both preclinical and clinical studies suggested that elevated oxidative and/or nitrative stress plays a key role in cardiac complications induced by hypercholesterolemia. Therefore, modulation of hypercholesterolemia-induced myocardial oxidative/nitrative stress is a feasible approach to prevent or treat deleterious cardiac consequences. In this review, we discuss the effects of various pharmaceuticals, nutraceuticals, some novel potential pharmacological approaches, and physical exercise on hypercholesterolemia-induced oxidative/nitrative stress and subsequent cardiac dysfunction as well as impaired ischemic stress adaptation of the heart in hypercholesterolemia.

show abstract

“…The function of OXPHOS was impaired by MIRI due to a series of enzymes, such as NADH oxidase or mitochondrial ROS release. Many studies have confirmed that increasing NAD + during MIRI could mitigate oxidative stress and alleviate myocardial injury ( Trueblood et al, 2000 ; Yamamoto et al, 2014 ; Tai et al, 2015 ). In the present study, the NA content significantly decreased after I/R, while the NA content increased after diazoxide postconditioning, indicating that diazoxide may exert protective effects by regulating NA and NAD + concentrations.…”

Section: Discussionmentioning

confidence: 98%

Metabolomics analysis in rat hearts with ischemia/reperfusion injury after diazoxide postconditioning

Xiang

Ren

et al. 2023

Front. Mol. Biosci.

View full text Add to dashboard Cite

Background: Diazoxide is a selective mitochondrial-sensitive potassium channel opening agent that has a definite effect on reducing myocardial ischemia/reperfusion injury (MIRI). However, the exact effects of diazoxide postconditioning on the myocardial metabolome remain unclear, which might contribute to the cardioprotective effects of diazoxide postconditioning.Methods: Rat hearts subjected to Langendorff perfusion were randomly assigned to the normal (Nor) group, ischemia/reperfusion (I/R) group, diazoxide (DZ) group and 5-hydroxydecanoic acid + diazoxide (5-HD + DZ) group. The heart rate (HR), left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), and maximum left ventricular pressure (+dp/dtmax) were recorded. The mitochondrial Flameng scores were analysed according to the ultrastructure of the ventricular myocardial tissue in the electron microscopy images. Rat hearts of each group were used to investigate the possible metabolic changes relevant to MIRI and diazoxide postconditioning.Results: The cardiac function indices in the Nor group were better than those in the other groups at the end point of reperfusion, and the HR, LVDP and +dp/dtmax of the Nor group at T2 were significantly higher than those of the other groups. Diazoxide postconditioning significantly improved cardiac function after ischaemic injury, and the HR, LVDP and +dp/dtmax of the DZ group at T2 were significantly higher than those of the I/R group, which could be abolished by 5-HD. The HR, LVDP and +dp/dtmax of the 5-HD + DZ group at T2 were significantly lower than those of the DZ group. The myocardial tissue in the Nor group was mostly intact, while it exhibited considerable damage in the I/R group. The ultrastructural integrity of the myocardium in the DZ group was higher than that in the I/R and 5-HD + DZ groups. The mitochondrial Flameng score in the Nor group was lower than that in the I/R, DZ and 5-HD + DZ groups. The mitochondrial Flameng score in the DZ group was lower than that in the I/R and 5-HD + DZ groups. Five metabolites, namely, L-glutamic acid, L-threonine, citric acid, succinate, and nicotinic acid, were suggested to be associated with the protective effects of diazoxide postconditioning on MIRI.Conclusion: Diazoxide postconditioning may improve MIRI via certain metabolic changes. This study provides resource data for future studies on metabolism relevant to diazoxide postconditioning and MIRI.

show abstract

Niacin Ameliorates Kidney Warm Ischemia and Reperfusion Injury–Induced Ventricular Dysfunction and Oxidative Stress and Disturbance in Mitochondrial Metabolism in Rats

Cited by 12 publications

References 17 publications

Overexpression of DJ-1 reduces oxidative stress and attenuates hypoxia/reoxygenation injury in NRK-52E cells exposed to high glucose

Overexpression of DJ-1 reduces oxidative stress and attenuates hypoxia/reoxygenation injury in NRK-52E cells exposed to high glucose

Modulation of Hypercholesterolemia‐Induced Oxidative/Nitrative Stress in the Heart

Metabolomics analysis in rat hearts with ischemia/reperfusion injury after diazoxide postconditioning

Contact Info

Product

Resources

About