scholarly journals C-REACTIVE PROTEIN OVEREXPRESSION EXACERBATES PRESSURE OVERLOAD-INDUCED CARDIAC REMODELING THROUGH ENHANCED INFLAMMATORY RESPONSE AND OXIDATIVE STRESS

2011 ◽  
Vol 57 (14) ◽  
pp. E534
Author(s):  
Toshiyuki Nagai ◽  
Toshihisa Anzai ◽  
Hidehiro Kaneko ◽  
Yoshinori Mano ◽  
Atsushi Anzai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Cardiac Remodeling ◽  
Pressure Overload ◽  
Protein Overexpression ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
And Oxidative Stress

scholarly journals C-Reactive Protein Overexpression Exacerbates Pressure Overload–Induced Cardiac Remodeling Through Enhanced Inflammatory Response

Hypertension ◽  
2011 ◽  
Vol 57 (2) ◽  
pp. 208-215 ◽  
Author(s):  
Toshiyuki Nagai ◽  
Toshihisa Anzai ◽  
Hidehiro Kaneko ◽  
Yoshinori Mano ◽  
Atsushi Anzai ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Cardiac Remodeling ◽  
Pressure Overload ◽  
Protein Overexpression ◽  
C Reactive Protein ◽  
Reactive Protein

Eicosapentaenoic acid suppresses adverse effects of C-reactive protein overexpression on pressure overload-induced cardiac remodeling

2012 ◽  
Vol 28 (3) ◽  
pp. 404-411 ◽  
Author(s):  
Toshiyuki Nagai ◽  
Toshihisa Anzai ◽  
Yoshinori Mano ◽  
Hidehiro Kaneko ◽  
Atsushi Anzai ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Eicosapentaenoic Acid ◽  
Cardiac Remodeling ◽  
Pressure Overload ◽  
Protein Overexpression ◽  
C Reactive Protein ◽  
Reactive Protein

scholarly journals Correlation of Ferritin and Transferrin Serum with hsCRP and F2-Isoprostane in Metabolic Syndrome

2010 ◽  
Vol 2 (3) ◽  
pp. 131
Author(s):  
Waode Nurfina ◽  
Irawan Yusuf ◽  
Mansyur Arif
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Iron Status ◽  
High Sensitivity ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
The Metabolic Syndrome ◽  
Metabolic Conditions ◽  
Inflammatory State ◽  
And Oxidative Stress

BACKGROUND: The low inflammatory state that accompanies the Metabolic Syndrome (MetS) associates with the overexpression of oxidative stress. Ferritin and Transferrin serum are often used to measure iron status and their concentrations are altered in several metabolic conditions. We hypothesized that concentration of Ferritin and Transferrin serum increase in Metabolic Syndrome (MetS) and correlate with the inflammation and oxidative stress.METHODS: We studied 65 male MetS patients, aged 43.26±7.16 years. Iron metabolism was measured by concentration of Ferritin and Transferrin serums, while inflammatory and oxidative stress by high sensitivity C-reactive Protein (hsCRP) and F2-Isoprostane.RESULTS: Concentration of Ferritin 315.70±188.63 ng/L and Transferrin 2.36±0.31 g/L increased along with increasing components of MetS. Concentration of Ferritin serum had a positive correlation with hsCRP (r=0.220) and F2-Isoprostane (r=0.023).CONCLUSION: Serum concentration of Ferritin increased in the MetS and correlates with hsCRP and F2-Isoprostane.KEYWORDS: metabolic syndrome, ferritin, transferrin, hsCRP, F2-isoprostane

scholarly journals Patients Undergoing Myeloablative Chemotherapy and Hematopoietic Stem Cell Transplantation Exhibit Depleted Vitamin C Status in Association with Febrile Neutropenia

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1879 ◽  
Author(s):  
Anitra C. Carr ◽  
Emma Spencer ◽  
Andrew Das ◽  
Natalie Meijer ◽  
Carolyn Lauren ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Febrile Neutropenia ◽  
Vitamin C ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
C Reactive Protein ◽  
Hematopoietic Stem ◽  
Reactive Protein ◽  
Myeloablative Chemotherapy ◽  
And Oxidative Stress

Patients undergoing myeloablative chemotherapy and hematopoietic stem cell transplantation (HSCT) experience profound neutropenia and vulnerability to infection. Previous research has indicated that patients with infections have depleted vitamin C status. In this study, we recruited 38 patients with hematopoietic cancer who were undergoing conditioning chemotherapy and HSCT. Blood samples were collected prior to transplantation, at one week, two weeks and four weeks following transplantation. Vitamin C status and biomarkers of inflammation (C-reactive protein) and oxidative stress (protein carbonyls and thiobarbituric acid reactive substances) were assessed in association with febrile neutropenia. The vitamin C status of the study participants decreased from 44 ± 7 µmol/L to 29 ± 5 µmol/L by week one (p = 0.001) and 19 ± 6 µmol/L by week two (p < 0.001), by which time all of the participants had undergone a febrile episode. By week four, vitamin C status had increased to 37 ± 10 µmol/L (p = 0.1). Pre-transplantation, the cohort comprised 19% with hypovitaminosis C (i.e., <23 µmol/L) and 8% with deficiency (i.e., <11 µmol/L). At week one, those with hypovitaminosis C had increased to 38%, and at week two, 72% had hypovitaminosis C, and 34% had outright deficiency. C-reactive protein concentrations increased from 3.5 ± 1.8 mg/L to 20 ± 11 mg/L at week one (p = 0.002), and 119 ± 25 mg/L at week two (p < 0.001), corresponding to the development of febrile neutropenia in the patients. By week four, these values had dropped to 17 ± 8 mg/L (p < 0.001). There was a significant inverse correlation between C-reactive protein concentrations and vitamin C status (r = −0.424, p < 0.001). Lipid oxidation (thiobarbituric acid reactive substances (TBARS)) increased significantly from 2.0 ± 0.3 µmol/L at baseline to 3.3 ± 0.6 µmol/L by week one (p < 0.001), and remained elevated at week two (p = 0.003), returning to baseline concentrations by week four (p = 0.3). Overall, the lowest mean vitamin C values (recorded at week two) corresponded with the highest mean C-reactive protein values and lowest mean neutrophil counts. Thus, depleted vitamin C status in the HSCT patients coincides with febrile neutropenia and elevated inflammation and oxidative stress.

4P-1056 Interrelationship between circulating C-reactive protein and oxidative stress in men

2003 ◽  
Vol 4 (2) ◽  
pp. 306-307
Author(s):  
O.Y. Kim ◽  
S.J. Goh ◽  
B.R. Cha ◽  
M.J. Wee ◽  
H. Cho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
And Oxidative Stress

C-reactive protein and oxidative stress in atrial fibrillation

2003 ◽  
Vol 88 (1) ◽  
pp. 103-104 ◽  
Author(s):  
Panagiotis Korantzopoulos ◽  
Dimitrios Galaris ◽  
Dimitrios Papaioannides ◽  
Stelianos Kokkoris
Keyword(s):  
Oxidative Stress ◽  
Atrial Fibrillation ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
And Oxidative Stress

scholarly journals Alleviation of Inflammation and Oxidative Stress in Pressure Overload-Induced Cardiac Remodeling and Heart Failure via IL-6/STAT3 Inhibition by Raloxifene

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Shengqi Huo ◽  
Wei Shi ◽  
Haiyan Ma ◽  
Dan Yan ◽  
Pengcheng Luo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Protein Expression ◽  
Cardiac Remodeling ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Stat3 Signaling ◽  
H9c2 Myoblasts ◽  
And Oxidative Stress ◽  
Stat3 Inhibition

Background. Inflammation and oxidative stress are involved in the initiation and progress of heart failure (HF). However, the role of the IL6/STAT3 pathway in the pressure overload-induced HF remains controversial. Methods and Results. Transverse aortic constriction (TAC) was used to induce pressure overload-HF in C57BL/6J mice. 18 mice were randomized into three groups (Sham, TAC, and TAC+raloxifene, n = 6 , respectively). Echocardiographic and histological results showed that cardiac hypertrophy, fibrosis, and left ventricular dysfunction were manifested in mice after TAC treatment of eight weeks, with aggravation of macrophage infiltration and interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) expression in the myocardium. TAC (four and eight weeks) elevated the phosphorylation of signal transducer and activator of transcription 3 (p-STAT3) and prohibitin2 (PHB2) protein expression. Importantly, IL-6/gp130/STAT3 inhibition by raloxifene alleviated TAC-induced myocardial inflammation, cardiac remodeling, and dysfunction. In vitro, we demonstrated cellular hypertrophy with STAT3 activation and oxidative stress exacerbation could be elicited by IL-6 (25 ng/mL, 48 h) in H9c2 myoblasts. Sustained IL-6 stimulation increased intracellular reactive oxygen species, repressed mitochondrial membrane potential (MMP), decreased intracellular content of ATP, and led to decreased SOD activity, an increase in iNOS protein expression, and increased protein expression of Pink1, Parkin, and Bnip3 involving in mitophagy, all of which were reversed by raloxifene. Conclusion. Inflammation and IL-6/STAT3 signaling were activated in TAC-induced HF in mice, while sustained IL-6 incubation elicited oxidative stress and mitophagy-related protein increase in H9c2 myoblasts, all of which were inhibited by raloxifene. These indicated IL-6/STAT3 signaling might be involved in the pathogenesis of myocardial hypertrophy and HF.

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