Similarities in serum oxidative stress markers and inflammatory cytokines in patients with overt schizophrenia at early and late stages of chronicity

2012 ◽  
Vol 46 (6) ◽  
pp. 819-824 ◽  
Author(s):  
Mariana Pedrini ◽  
Raffael Massuda ◽  
Gabriel R. Fries ◽  
Matheus A. de Bittencourt Pasquali ◽  
Carlos Eduardo Schnorr ◽  
...  
2021 ◽  
Vol 14 (4) ◽  
pp. 380
Author(s):  
Hadeel Alsaegh ◽  
Hala Eweis ◽  
Fatemah Kamal ◽  
Aziza Alrafiah

The risk of developing epilepsy is strongly linked to peripheral inflammatory disorders in humans. High-mobility group box protein 1 (HMGB1) has the most focus for being a suspect in this scenario. The current study aimed to detect the celecoxib effect, an anti-inflammatory drug, on decreasing seizure susceptibility and organ damage in lipopolysaccharides (LPS)/pilocarpine (PILO) pretreated Wistar rats. Rats were divided into 6 groups (8 each): group 1 (control), group 2 (PILO), group 3 (PILO+LPS), group 4 (PILO+LPS+(VPA) Valproic acid), group 5 (PILO+LPS+Celecoxib), and group 6 (PILO+LPS+VPA+Celecoxib). LPS was used to induce sepsis and PILO to induce seizures. Oxidative stress markers, pro-inflammatory cytokines, and HMGB1 levels in serum and brain homogenate were evaluated. Histopathological studies were conducted on the hippocampus, liver, lung, and kidney. Treatment with celecoxib either alone or in combination with VPA significantly reduced Racine score and delays latency to generalized tonic-clonic seizures onset with a significant decrease in hippocampal levels of pro-inflammatory cytokines, oxidative stress markers, and increase in reduced glutathione. In addition, celecoxib treatment either alone or in combination with VPA suppressed HMGB1translocation into peripheral circulation more than treatment with VPA alone. Furthermore, hippocampus, liver, lung, and kidney histopathological changes were improved in contrast to other epileptic groups. Celecoxib either alone or combined with VPA has antiepileptic and multiorgan protective effects on acute seizures and inflammatory models induced by PILO with LPS. It decreased histopathological findings, oxidative, and inflammatory effects induced by VPA and LPS. This might be due to its anti-oxidative, anti-inflammatory and anti-HMGB1 mediated effects.


2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Suzan A. Khodir ◽  
Rehab M. Samaka ◽  
Omnia Ameen

Introduction. Not only is diabetic nephropathy (DN) the most common cause of end-stage renal disease worldwide, but it also increases the risk of mortality up to fourteen times compared to normoalbuminuric diabetic patients. Aim. The aim of the current study was the evaluation of the renoprotective effects of vitamin D in DN and the possible interplay between autophagy and mTOR pathways. Materials and Methods. Fifty male Wistar albino rats were divided (10/group) into control, DN group, insulin-treated DN group, vitamin D-treated DN group, and combined insulin and vitamin D-treated DN group. Assessments of systolic blood pressure, albuminuria, creatinine clearance, serum glucose, insulin, urea, creatinine, inflammatory cytokines, oxidative stress markers, and rat kidney gene expression of mTOR were performed. Histopathological and immunohistochemical assessments of autophagy marker LC3 in rat kidneys were also performed. Results. DN was associated with significant increases in SBP, urinary albumin, serum glucose, urea, creatinine, inflammatory cytokines, MDA, and mTOR gene expression (P<0.05). However, there was significant decrease in creatinine clearance, serum insulin, GSH, and H score value of LC3 when compared with control group (P<0.05). The combination of insulin and vitamin D treatment significantly restored DN changes when compared with the other treated groups, except in oxidative stress markers where there was an insignificant difference between the combination-treated and insulin-treated groups (P>0.05). Conclusion. It has been concluded that vitamin D is a potent adjuvant therapy in treatment of DN via downregulation of mTOR gene expression, stimulation of autophagy, and antioxidant, anti-inflammatory, and hypotensive effects.


2019 ◽  
Vol 17 ◽  
pp. 205873921984554
Author(s):  
Zhiming Song ◽  
Paul Weigl ◽  
Bi Wang

This study aimed to analyze the correlations of inflammatory cytokines, oxidative stress markers, and matrix metalloproteinases (MMPs) in gingival crevicular fluid (GCF) with peri-implantitis (PI). Forty patients receiving dental implantation were enrolled. There were 52 implants, which were divided into PI group (42 implants) and health implant (HI) group (10 implants). Fifty-two healthy teeth (HT) with the same names with affected teeth in the patients were selected as the control group. The periodontal status was recorded. The GCF was collected and quantified. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), hypersensitive C-reactive protein (hs-CRP), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), MMP-13, and MMP-8 were detected using enzyme-linked immunosorbent assay (ELISA). Results showed that the probing depth, sulcus bleeding index, GCF volume, and TNF-α, IL-6, hs-CRP, MMP-8, and MMP-13 levels in GCF in PI group were significantly higher than HI and HT groups, respectively ( P < 0.01 or P < 0.05). The SOD and GSH-Px levels in PI group were significantly lower than HI and HT groups, respectively ( P < 0.05). Excepting hs-CRP, there was no significant difference of each index between HI and HT groups ( P > 0.05). In conclusion, TNF-α, IL-6, hs-CRP, SOD, GSH-Px, MMP-8, and MMP-13 are involved in the occurrence of PI, and they may be used as auxiliary indicators to evaluate the degree of PI. In addition, the clinical periodontal index probing depth and sulcus bleeding index are positively correlated with GCF volume, hs-CRP, MMP-8, and MMP-13.


2020 ◽  
Vol 7 ◽  
Author(s):  
Elodia Nataly Díaz-De la Cruz ◽  
José Ignacio Cerrillos-Gutiérrez ◽  
Andrés García-Sánchez ◽  
Jorge Andrade-Sierra ◽  
Ernesto Germán Cardona-Muñoz ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Shamma Al-Muraikhy ◽  
Manjunath Ramanjaneya ◽  
Alexander S. Dömling ◽  
Ilham Bettahi ◽  
Francesco Donati ◽  
...  

Introduction: Aerobic exercise activates the complement system in the peripheral blood. However, the effect of age and high intensity endurance training on the levels of circulating complements and sassociated inflammatory cytokines, oxidative stress markers and cellular aging remains unknown.Methods: In this study, serum samples from 79 elite athletes who belong to high (n = 48) and low/moderate (n = 31) endurance sports and two age groups (below 30 years old, n = 53, and above 30 years old, n = 26) were profiled for 14 complements. Linear models were used to assess differences in complements levels between sport and age groups. Spearmann’s correlation was used to assess the relationship among detected complements and proinflammatory cytokines, oxidative stress markers and telomere lengths.Results: High endurance elite athletes exhibited significantly lower levels of circulating C2, C3b/iC3b and adipsin complements than their age-matched low/moderate endurance counterparts. Levels of C2, adipsin and C3b/iC3b were positively correlated with most detected complements, the pro-inflammatory cytokines TNF-alpha and IL-22 and the anti-oxidant enzyme catalase. However, they were negatively correlated with telomere length only in younger elite athletes regardless of their sport groups. Furthermore, high endurance elite athletes showed significantly lower concentrations of C3b/iC3b, C4b, C5, C5a, C1q, C3, C4, factor H and properdin in younger athletes compared to their older counterparts.Conclusion: Our novel data suggest that high endurance elite athletes exhibit age-independent lower levels of circulating C2, C3b/iC3b and adipsin, associated with lower inflammatory, oxidative stress and cellular aging, as well as lower levels of 10 other complements in younger athletes compared to older counterparts. Assessing the effect of various levels of endurance sports on complements-based immune response provides a better understanding of exercise physiology and pathophysiology of elite athletes.


2018 ◽  
Vol 49 (6) ◽  
pp. 391-398 ◽  
Author(s):  
Angélica L. Sánchez-López ◽  
Genaro Gabriel Ortiz ◽  
Fermín P. Pacheco-Moises ◽  
Mario A. Mireles-Ramírez ◽  
Oscar K. Bitzer-Quintero ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document