scholarly journals TNF-α gene promoter polymorphism at nucleotide −308 and the inflammatory response and oxidative stress induced by cardiac surgery: role of heart failure and medical treatment☆

2008 ◽  
Vol 34 (2) ◽  
pp. 332-337 ◽  
Author(s):  
Manuel Galiñanes ◽  
Martha James ◽  
Veryan Codd ◽  
Amar Baxi ◽  
Leonidas Hadjinikolaou
Author(s):  
Byoung Yong Ahn ◽  
Kyoung Ah Kim ◽  
Hae Yun Nam ◽  
Je Hyeok Mun ◽  
Jin Sook Jeoung ◽  
...  

2020 ◽  
Vol 25 (40) ◽  
pp. 4310-4317 ◽  
Author(s):  
Lichao Sun ◽  
Shouqin Ji ◽  
Jihong Xing

Background/Aims: Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits after transient global ischemia induced by cardiac arrest (CA). The present study was to examine the role of microRNA- 155 (miR-155) in regulating IL-1β, IL-6 and TNF-α in the hippocampus of rats with induction of CA. We further examined the levels of products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, indication of oxidative stress); and 8-hydroxy-2’-deoxyguanosine (8-OHdG, indication of protein oxidation) after cerebral inhibition of miR-155. Methods: CA was induced by asphyxia and followed by cardiopulmonary resuscitation in rats. ELISA and western blot analysis were used to determine the levels of PICs and products of oxidative stress; and the protein expression of NADPH oxidase (NOXs) in the hippocampus. In addition, neurological severity score and brain edema were examined to assess neurological functions. Results: We observed amplification of IL-1β, IL-6 and TNF-α along with 8-iso PGF2α and 8-OHdG in the hippocampus of CA rats. Cerebral administration of miR-155 inhibitor diminished upregulation of PICs in the hippocampus. This also attenuated products of oxidative stress and upregulation of NOX4. Notably, inhibition of miR-155 improved neurological severity score and brain edema and this was linked to signal pathways of PIC and oxidative stress. Conclusion: We showed the significant role of blocking miR-155 signal in improving the neurological function in CA rats likely via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting that miR-155 may be a target in preventing and/or alleviating development of the impaired neurological functions during CA-evoked global cerebral ischemia.


2010 ◽  
Vol 18 (3) ◽  
pp. 880-887 ◽  
Author(s):  
Rohit Upadhyay ◽  
Rohini Khurana ◽  
Shaleen Kumar ◽  
Uday Chand Ghoshal ◽  
Balraj Mittal

2014 ◽  
Vol 20 (5) ◽  
pp. 309 ◽  
Author(s):  
Venkateshwari Ananthapur ◽  
AmarChand Bhayal ◽  
Krishnaveni Devulapalli ◽  
Ramanna Macherla ◽  
Pratibha Nallari ◽  
...  

2012 ◽  
Vol 31 (7) ◽  
pp. 1051-1057 ◽  
Author(s):  
Quan-ming Zhao ◽  
Xiong Guo ◽  
Jiang-hua Lai ◽  
Wu-hong Tan ◽  
Wei-zhuo Wang ◽  
...  

Author(s):  
SANDEEP DAS ◽  
DIPAYAN CHOUDHURI

Objective: Emerging evidence established the role of dietary calcium in the modulation of obesity. Obesity is known to induce inflammatory and oxidative stress in adipocytes resulting in several metabolic complications. In the present study, we evaluated the role of low and high calcium diet on systemic inflammatory response and oxidative stress markers in both plasma and hepatic tissues in male rats. Methods: A total of 30 male rats were divided into three groups and fed with control, low calcium (0.25%), and high calcium (1.0%) diet for 3 months. All the diets were isocaloric in nature. At the end of the treatment, all rats were sacrificed, followed by collection of blood and hepatic tissue for inflammatory, oxidative, antioxidant, and histological study. Results: Rats fed with a low calcium diet showed a significant increase in the body weight gain, liver mass, plasma inflammatory markers C-reactive protein, interleukin-6, and tumor necrosis factor-alpha. Low calcium diet significantly increased the lipid peroxidation and protein carbonylation and decreased the superoxide dismutase and glutathione peroxidase activities in both plasma and liver. High calcium diet, on the other hand, showed the reversed effect. Conclusion: Low calcium in the diet, along with obesity, increases the systemic inflammatory response, which in turn increases oxidative stress both in blood and hepatic tissues. This might be associated with obesity-induced hepatic disorder. High calcium in diet attenuates this effect.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Neuza Costa ◽  
Thaisa Verediano ◽  
Mirelle Viana ◽  
Maria Vaz-Tostes

Abstract Objectives To investigate the prebiotic effect of yacon, source of fructooligosaccharides (FOS), on the integrity of the intestinal barrier, inflammatory response and oxidative stress in rats with induced colon cancer. Methods 44 adult Wistar rats were distributed into 4 groups: S (without colon cancer and yacon; n = 10); C (with colon cancer without yacon; n = 12); Y (without colon cancer with yacon; n = 10); and CY (with colon cancer and yacon; n = 12). Animals of groups S and C received AIN-93 M diet and animals of groups Y and CY received the same diet but added with yacon flour containing 28.95% FOS, to provide 5% FOS in the diet, for 16 weeks. From week 4 to 8, the animals of C and CY groups received an intraperitoneal dose of 25 mg/kg body weight of 1.2-dimethylhydrazine (DMH-Sigma®) once a week. In the last week, 24h-urine collection was performed for intestinal permeability analysis using lactulose and mannitol. Blood sample was collected for the analysis of IL-10 and IL-12 cytokines (Milliplex® Map, Luminex®) and total antioxidant capacity - TAC (Elabscience®). Large intestine was collected for intraluminal pH, short chain fatty acids - SCFA (HPLC) and immunoglobulin A – sIgA (Cloud-Clone®) analysis. Normal distributed data were analyzed by Two-way ANOVA, followed by Newman-Keuls (p < 0.05), using GraphPad Prism®, version 7. Results Cancer-induced animals showed higher TNF-α, SCFA (acetate, propionate and butirate), and lower TAC. Yacon reduced intraluminal pH and lactulose/mannitol ratio, increased propionic acid in the feces, but showed no effect on IL-10, IL-12, TNF-α, and IL-10/IL-12 ratio. The levels of sIgA were increased only in the group fed yacon without cancer (group Y). Mannitol and TAC were higher in CY group, showing a significant interaction of yacon and colon cancer. Conclusions Yacon reduced pH, intestinal permeability and the oxidative stress associated with colon cancer. The local immunity (sIgA) was raised, although no effect was observed on cytokines with yacon consumption. Yacon is a rich source of FOS wich improves the intestinal barrier and mucosal immunity, particularly in healthy animals. Funding Sources CNPq, FAPES.


Sign in / Sign up

Export Citation Format

Share Document