scholarly journals Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines

10.3791/57879 ◽  
2021 ◽  
Author(s):  
Muammer Üçal ◽  
Michaela Tanja Haindl ◽  
Milena Z. Adzemovic ◽  
Manuel Zeitelhofer ◽  
Ute Schaefer ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Rat Model ◽  
Intracerebral Injection ◽  
Pro Inflammatory Cytokines

scholarly journals Hepatoprotective effect ofCommiphora myrrhaagainstd-GalN/LPS-induced hepatic injury in a rat model through attenuation of pro inflammatory cytokines and related genes

2015 ◽  
Vol 53 (12) ◽  
pp. 1759-1767 ◽  
Author(s):  
Ajaz Ahmad ◽  
Mohammad Raish ◽  
Majid A. Ganaie ◽  
Syed Rizwan Ahmad ◽  
Kazi Mohsin ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Rat Model ◽  
Hepatic Injury ◽  
Hepatoprotective Effect ◽  
Pro Inflammatory Cytokines

The involvement of pro-inflammatory cytokines in nephrogenic systemic fibrosis – A mechanistic hypothesis based on preclinical results from a rat model treated with gadodiamide

2009 ◽  
Vol 61 (6) ◽  
pp. 537-552 ◽  
Author(s):  
T. Steger-Hartmann ◽  
M. Raschke ◽  
B. Riefke ◽  
H. Pietsch ◽  
M.A. Sieber ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Rat Model ◽  
Nephrogenic Systemic Fibrosis ◽  
Pro Inflammatory Cytokines

Escitalopram reduces circulating pro-inflammatory cytokines and improves depressive behavior without affecting sleep in a rat model of post-cardiac infarct depression

2011 ◽  
Vol 225 (1) ◽  
pp. 243-251 ◽  
Author(s):  
Thierno Madjou Bah ◽  
Mohamed Benderdour ◽  
Sévan Kaloustian ◽  
Ramy Karam ◽  
Guy Rousseau ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Rat Model ◽  
Depressive Behavior ◽  
Pro Inflammatory Cytokines

scholarly journals Roselle Seed Oil and its Nano-Formulation Alleviated Oxidative Stress, Activated Nrf2 and Downregulated m-RNA Expression Genes of Pro-inflammatory Cytokines in Paracetamol-intoxicated Rat Model

2019 ◽  
Vol 14 (1) ◽  
pp. 1-17 ◽  
Author(s):  
Mai E. Hussein ◽  
Amira S. El Senousy ◽  
Wessam H. Abd-elsalam ◽  
Kawkab A. Ahmed ◽  
Hesham I. El-askary ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Rat Model ◽  
Seed Oil ◽  
Rna Expression ◽  
Nano Formulation ◽  
Pro Inflammatory Cytokines

miR-211-5p contributes to chondrocyte differentiation by suppressing Fibulin-4 expression to play a role in osteoarthritis

2019 ◽  
Vol 166 (6) ◽  
pp. 495-502 ◽  
Author(s):  
Hao Liu ◽  
Jun Luo
Keyword(s):  
Inflammatory Cytokines ◽  
Rat Model ◽  
Cartilage Matrix ◽  
Chondrocyte Differentiation ◽  
Matrix Degradation ◽  
Downstream Target ◽  
Promising Target ◽  
Human Disorders ◽  
Pro Inflammatory Cytokines

Abstract MicroRNAs (miRNAs) serve as key regulators in human disorders. Previous research reported that miR-211-5p is down-regulated in osteoarthritis (OA) and that Fibulin-4 inhibits chondrocyte differentiation. However, the role of miR-211-5p in the development of OA has not been clarified, and its downstream target has not been studied. This study aimed to explore the effect of miR-211-5p on chondrocyte differentiation and its influence on OA pathogenesis, as well as the interaction between miR-211-5p and Fibulin-4. In this study, we found that miR-211-5p is significantly down-regulated in articular cartilage tissues in an OA rat model, whereas it is clearly up-regulated during chondrocyte differentiation of ATDC5 cells. Silencing miR-211-5p in ATDC5 cells had an adverse effect on chondrocyte differentiation. Fibulin-4 was identified as a target of miR-211-5p, and miR-211-5p participated in chondrocyte differentiation by negatively regulating Fibulin-4 expression. In the OA rat model, miR-211-5p overexpression facilitated chondrocyte differentiation, along with the reduced pro-inflammatory cytokines level and the level of proteinases responsible for cartilage matrix degradation. In summary, miR-211-5p promotes chondrocyte differentiation by negatively regulating Fibulin-4 expression, and represses the expression of pro-inflammatory cytokines and proteinases responsible for cartilage matrix degradation in OA. miR-211-5p may serve as a promising target for OA treatment.

scholarly journals A rat model of mild intestinal inflammation induced byStaphylococcus aureusenterotoxin B

2010 ◽  
Vol 69 (3) ◽  
pp. 447-453 ◽  
Author(s):  
Anna Pérez-Bosque ◽  
Miquel Moretó
Keyword(s):  
T Lymphocytes ◽  
Inflammatory Cytokines ◽  
Rat Model ◽  
Plasma Proteins ◽  
Intestinal Inflammation ◽  
Killer Cell ◽  
Peyer's Patches ◽  
Peyer’S Patches ◽  
Activated T Lymphocytes ◽  
Pro Inflammatory Cytokines

The epithelial barrier of the intestine and the gut-associated lymphoid tissue (GALT) protects the host against luminal pathogenic micro-organisms. This is important at weaning, when animals are exposed to infectious agents and stresses. We have developed a rat model of intestinal inflammation post weaning, based on the systemic administration ofStaphylococcus aureusenterotoxin B (SEB). Since the inflammatory response obtained is mild, the food intake pattern is not affected, which makes this model useful for studies of nutritional therapies for intestinal inflammatory disease. SEB increased T-lymphocytes in Peyer's patches and the number of activated T-lymphocytes in mesenteric lymph nodes (organized GALT). In the lamina propria, SEB increased activated T-lymphocytes as well as cytotoxic and natural killer-cell populations of the diffuse GALT. It also increased pro-inflammatory cytokines and inflammatory mediators in both Peyer's patches and mucosa. Rats given SEB had higher paracellular permeability to macromolecules, which was associated with a reduction in epithelial tightness. This model was used to examine whether dietary supplementation with spray-dried animal plasma proteins affects intestinal inflammation. Results showed that dietary plasma proteins can attenuate the mucosal immune response in both organized and diffuse GALT and that these effects are mediated by a reduction in the production of pro-inflammatory cytokines.

scholarly journals Effect of 1,25-(OH)2D3 on Proliferation of Fibroblast-Like Synoviocytes and Expressions of Pro-Inflammatory Cytokines through Regulating MicroRNA-22 in a Rat Model of Rheumatoid Arthritis

2017 ◽  
Vol 42 (1) ◽  
pp. 145-155 ◽  
Author(s):  
Ping Fan ◽  
Lan He ◽  
Nan Hu ◽  
Jing Luo ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Inflammatory Cytokines ◽  
Rat Model ◽  
Type Ii Collagen ◽  
Proliferation Inhibition ◽  
Blank Group ◽  
Mtt Method ◽  
Cox 2 ◽  
Fibroblast Like Synoviocytes ◽  
Pro Inflammatory Cytokines

Objective: This study aims to investigate the regulatory mechanism of 1,25-(OH)2D3 on the proliferation of fibroblast-like synoviocytes (FLS) and expressions of pro-inflammatory cytokines in rheumatoid arthritis (RA) rats via microRNA-22 (miR-22). Methods: A rat model of RA was established with a subcutaneous injection of type II collagen. After treated with different concentrations of 1,25-(OH)2D3 the proliferation of FLS was estimated by the MTT method, and the optimal concentration of 1,25-(OH)2D3 was selected for further experiments. Cell proliferation was detected by MTT. Cell cycle and apoptosis were analyzed by FCM. The IL-1β, IL-6, IL-8, and PGE2 protein expressions were determined by ELISA, and MMP-3, INOS, and Cox-2 mRNA expressions were measured by qRT-PCR. Results: The rat model of RA was successfully established. Compared with the blank group, the 1,25-(OH)2D3 and miR-22 inhibitors groups exhibited higher proliferation inhibition and apoptosis rates, lower levels of pro-inflammatory cytokines (IL-1β, IL-6, IL-8, and PGE2), and decreased mRNA expressions of MMP-3, INOS, and Cox-2. The miR-22 mimics group had lower proliferation inhibition and apoptosis rates, elevated expressions of pro-inflammatory cytokines and MMP-3, INOS, and Cox-2 than the blank group. In contrast to the 1,25-(OH)2D3 group, the proliferation inhibition and apoptosis rates were down-regulated, and the expressions of pro-inflammatory cytokines and MMP-3, INOS, and Cox-2 were up-regulated in the 1,25-(OH)2D3 + miR-22 mimics group. Conclusion: Our study demonstrated that 1,25-(OH)2D3 inhibits the proliferation of FLS and alleviates inflammatory response in RA rats by down-regulating miR-22.

Sign in / Sign up

Export Citation Format

Share Document