PS 02-36 A BIOMARKER OF TISSUE DAMAGE, LACTATE DEHYDROGENASE, IS ASSOCIATED WITH FIBULIN-1 AND OXIDATIVE STRESS IN BLACK SOUTH AFRICANS

Although substance P (SP) has been implicated as a mediator of neurogenic inflammation in the small intestine, little information is available regarding the role of SP in the pathogenesis of chronic ulcerative colitis. In this study, our aim was to investigate whether the intraperitoneal administration of a nonpeptide neurokinin-1 (NK-1) antagonist, CP-96345, which antagonizes the binding of SP to its NK-1 receptor, results in the attenuation of colonic inflammation induced in rats by 5% dextran sodium sulfate (DSS) in drinking water for 10 days compared with an inactive enantiomer, CP-96344. Disease activity was assessed daily for 10 days, after which colonic tissue damage was scored and myeloperoxidase activity and colon and urinary 8-isoprostanes were measured. Animals receiving DSS exhibited marked physical signs of colitis by day 5 compared with controls. Chronic administration of the NK-1 antagonist significantly reduced the disease activity index, mucosal myeloperoxidase activity, colonic tissue damage score, and mucosal and urinary levels of 8-isoprostanes compared with inactive enantiomer- or vehicle-injected (saline) animals receiving DSS alone. These data indicate that the administration of an NK-1 antagonist can attenuate colonic inflammation and oxidative stress and suggest a novel therapeutic approach in the treatment of chronic ulcerative colitis.

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Connecting Glycolytic Enzymes, Microtubules and Oxidative Stress: Cysteine Oxidation of Pyruvate Kinase and Lactate Dehydrogenase and Its Effects on Enzyme Activity

Free Radical Biology and Medicine ◽

10.1016/j.freeradbiomed.2015.10.384 ◽

2015 ◽

Vol 87 ◽

pp. S149

Author(s):

Lisa MLandino ◽

Taylor K Lain ◽

Jessica L Joyce ◽

Lydia E Boike

Keyword(s):

Oxidative Stress ◽

Enzyme Activity ◽

Lactate Dehydrogenase ◽

Pyruvate Kinase ◽

Glycolytic Enzymes ◽

Cysteine Oxidation ◽

And Oxidative Stress

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Levels of Proinflammatory Cytokines, Oxidative Stress, and Tissue Damage Markers in Patients with Acute Heart Failure with and without Cardiorenal Syndrome Type 1

Cardiorenal Medicine ◽

10.1159/000492602 ◽

2018 ◽

Vol 8 (4) ◽

pp. 321-331 ◽

Cited By ~ 9

Author(s):

Grazia Maria Virzì ◽

Andrea Breglia ◽

Alessandra Brocca ◽

Massimo de Cal ◽

Chiara Bolin ◽

...

Keyword(s):

Oxidative Stress ◽

Heart Failure ◽

Proinflammatory Cytokines ◽

Tissue Damage ◽

Cardiorenal Syndrome ◽

Syndrome Type ◽

Spearman's Rho ◽

Spearman’S Rho ◽

And Oxidative Stress

Background: Cardiorenal syndrome type 1 (CRS type 1) is characterized by a rapid worsening of cardiac function leading to acute kidney injury (AKI). Inflammation and oxidative stress seem to play a pivotal role in its pathophysiology. In this in vivo study, we examined the putative role of inflammation and humoral markers in the pathogenesis of the CRS type 1. Methods: We enrolled 53 patients with acute heart failure (AHF); 17 of them developed AKI (CRS type 1). The cause of AKI was presumed to be related to cardiac dysfunction after having excluded other causes. We assessed the plasma levels of proinflammatory cytokines (TNF-α, IL-6, IL-18, sICAM, RANTES, GMCSF), oxidative stress marker (myeloperoxidase, MPO), brain natriuretic peptide (BNP), and neutrophil gelatinase-associated lipocalin (NGAL) in AHF and CRS type 1 patients. Results: We observed a significant increase in IL-6, IL-18, and MPO levels in CRS type 1 group compared to AHF (p < 0.001). We found higher NGAL at admission in the CRS type 1 group compared to the AHF group (p = 0.008) and a positive correlation between NGAL and IL-6 (Spearman’s rho = 0.45, p = 0.003) and between IL-6 and BNP (Spearman’s rho = 0.43, p = 0.004). We observed lower hemoglobin levels in CRS type 1 patients compared to AHF patients (p < 0.05) and inverse correlation between hemoglobin and cytokines (IL-6: Spearman’s rho = –0.38, p = 0.005; IL-18: Spearman’s rho = –0.32, p = 0.02). Conclusion: Patients affected by CRS type 1 present increased levels of proinflammatory cytokines and oxidative stress markers, increased levels of tissue damage markers, and lower hemoglobin levels. All these factors may be implicated in the pathophysiology of CRS type 1 syndrome.

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Carvacrol attenuates cyclophosphamide-induced oxidative stress in rat kidney

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2016-0450 ◽

2017 ◽

Vol 95 (7) ◽

pp. 844-849 ◽

Cited By ~ 5

Author(s):

Sibel Gunes ◽

Adnan Ayhanci ◽

Varol Sahinturk ◽

Diler Us Altay ◽

Ruhi Uyar

Keyword(s):

Oxidative Stress ◽

Superoxide Dismutase ◽

Oxidative Damage ◽

Tissue Damage ◽

Total Antioxidant Capacity ◽

Rat Kidney ◽

Control Group ◽

Antioxidative Effect ◽

Total Antioxidant ◽

And Oxidative Stress

Cyclophosphamide (CP) is an antineoplastic drug that induces kidney damage via producing oxidative stress. Carvacrol (CAR) has antioxidative effect and we postulated that it can be protective against CP-induced nephrotoxicity. Six groups (n = 7) of rats (control, 100 mg/kg CP, CP+5 mg/kg CAR, CP+10 mg/kg CAR, 5 mg/kg CAR, and 10 mg/kg CAR) were injected intraperitoneally. Serum malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), creatinine (CRE), total antioxidant capacity (TAC), and total oxidant state (TOS) were measured, and oxidative stress indexes (OSI) were calculated. Kidneys were also analyzed histologically. In CP-alone group MDA, CRE, TOS, and OSI levels increased whereas GSH, SOD, CAT, and TAC levels decreased compared with control group. In CP plus CAR groups, MDA, TOS, and OSI levels decreased whereas GSH, SOD, CAT, and TAC levels increased compared with CP-alone group. However, CRE levels were similar in CP-alone and CP+5 CAR group whereas decreased in CP+10 CAR group. CP+10 CAR group was significantly different in all parameters (except TAC) from CP+5 CAR group. Kidney microscopy was showed lower tissue damage in CP plus CAR groups. In conclusion, 10 mg/kg CAR is more effective than 5 mg/kg CAR in prevention of CP-induced oxidative damage on kidney.

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