Interaction among extracellular nicotinamide phosphoribosyltransferase, toll‐like receptor‐4, and inflammatory cytokines in pre‐eclampsia

2021 ◽  
Author(s):  
Priscila R. Nunes ◽  
Carla S. Ceron ◽  
Marcelo R. Luizon ◽  
Valeria C. Sandrim
Keyword(s):  
Inflammatory Cytokines ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Nicotinamide Phosphoribosyltransferase

Toll‐like receptor 4 polymorphisms were associated with low serum pro‐inflammatory cytokines in BCG osteitis survivors

2019 ◽  
Vol 109 (7) ◽  
pp. 1417-1422 ◽  
Author(s):  
Matti Korppi ◽  
Johanna Teräsjärvi ◽  
Eero Lauhkonen ◽  
Heini Huhtala ◽  
Kirsi Nuolivirta ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Low Serum ◽  
Pro Inflammatory Cytokines

Effects of local lipopolysaccharide administration on the expression of Toll-like receptor 4 and pro-inflammatory cytokines in uterus and oviduct of rabbit does

2018 ◽  
Vol 107 ◽  
pp. 162-174 ◽  
Author(s):  
Laura Menchetti ◽  
Olimpia Barbato ◽  
Iulia Elena Filipescu ◽  
Giovanna Traina ◽  
Leonardo Leonardi ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Pro Inflammatory Cytokines

scholarly journals TAK-242, an Antagonist for Toll-like Receptor 4, Protects against Acute Cerebral Ischemia/Reperfusion Injury in Mice

2015 ◽  
Vol 35 (4) ◽  
pp. 536-542 ◽  
Author(s):  
Fang Hua ◽  
Huiling Tang ◽  
Jun Wang ◽  
Megan C Prunty ◽  
Xiaodong Hua ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Inflammatory Cytokines ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Artery Occlusion ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Tlr4 Signaling ◽  
Cerebral Ischemia Reperfusion ◽  
Acute Cerebral Ischemia

Toll-like receptor 4 (TLR4) contributes to cerebral ischemia/reperfusion (I/R) injury and is a potential target for the treatment of ischemic stroke. This experiment is to evaluate the effect of an exogenous TLR4 antagonist, TAK-242, against acute cerebral I/R injury. A mouse model of cerebral I/R was induced by transient middle cerebral artery occlusion. TAK-242 (3 mg/kg body weight) was injected intraperitoneally 1 hour after ischemia. Our results showed that the concentration of TAK-242 in plasma increased to 52.0 ng/mL 3 hours after injection, was maintained at 54.1 ng/mL 8 hours after injection, and decreased to 22.6 ng/mL 24 hours after injection. The concentration of TAK-242 in brain tissue increased to 26.1 ng/mL in ischemic hemisphere and 14.2 ng/mL in nonischemic hemisphere 3 hours after injection, and was maintained at the similar levels 24 hours after injection. We found that TAK-242 significantly reduced cerebral infarction compared with vehicle control, improved neurologic function, inhibited the phosphorylation of downstream protein kinases in TLR4 signaling pathway, and downregulated the expression of inflammatory cytokines. We conclude that TAK-242 is able to cross blood-brain barrier, blocks TLR4 signaling, mediates the expression of inflammatory cytokines, and protects the brain from acute damage induced by I/R.

scholarly journals Astragaloside IV alleviates placental oxidative stress and inflammation in GDM mice

2020 ◽  
Vol 9 (9) ◽  
pp. 939-945
Author(s):  
Ling Zhou ◽  
Ruixue Zhang ◽  
Shuangyan Yang ◽  
Yaguang Zhang ◽  
Dandan Shi
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Protective Role ◽  
The Other ◽  
Toll Like Receptor ◽  
Astragaloside Iv ◽  
Toll Like Receptor 4 ◽  
Pregnant Mice ◽  
Placental Oxidative Stress

Background: Our previous study revealed that astragaloside IV (AS-IV) effectively improved gestational diabetes mellitus (GDM) by reducing hepatic gluconeogenesis. Due to the importance of placental oxidative stress, we further explored the protective role of AS-IV on placental oxidative stress in GDM. Methods: First, non-pregnant mice were orally administrated with AS-IV to evaluate its safety and effect. Then GDM mice were orally administered with AS-IV for 20 days and its effect on the symptoms of GDM, placental oxidative stress, secretions of inflammatory cytokines, as well as toll-like receptor 4 (TLR4)/NF-κB signaling pathway, were evaluated. Results: AS-IV had no adverse effect on non-pregnant mice. On the other hand, AS-IV significantly attenuated the GDM-induced hyperglycemia, glucose intolerance, insulin resistance, placental oxidative stress, productions of inflammatory cytokines and the activation of TLR4/NF-κB pathway. Conclusion: AS-IV effectively protected against GDM by alleviating placental oxidative stress and inflammation, in which TLR4/NF-κB might be involved.

scholarly journals Effects of Adipose-Derived Biogenic Nanoparticle-Associated microRNA-451a on Toll-like Receptor 4-Induced Cytokines

Pharmaceutics ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 16
Author(s):  
Xinghua Wang ◽  
Anthony Pham ◽  
Lu Kang ◽  
Sierra A. Walker ◽  
Irina Davidovich ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Signaling Pathways ◽  
Extracellular Vesicles ◽  
Inflammatory Cytokines ◽  
Stromal Cells ◽  
Toll Like Receptor ◽  
Immunomodulatory Effects ◽  
Toll Like Receptor 4 ◽  
Biogenic Nanoparticles ◽  
Pro Inflammatory Cytokines

Extracellular vesicles (EVs) are cell-released nanoparticles that transfer biomolecular content between cells. Among EV-associated biomolecules, microRNAs (miRNAs/miRs) represent one of the most important modulators of signaling pathways in recipient cells. Previous studies have shown that EVs from adipose-derived mesenchymal stromal cells (MSCs) and adipose tissue modulate inflammatory pathways in macrophages. In this study, the effects of miRNAs that are abundant in adipose tissue EVs and other biogenic nanoparticles (BiNPs) were assessed in terms of altering Toll-like receptor 4 (TLR4)-induced cytokines. TLR-4 signaling in macrophages is often triggered by pathogen or damage-induced inflammation and is associated with several diseases. This study demonstrates that miR-451a, which is abundant in adipose tissue BiNPs, suppresses pro-inflammatory cytokines and increases anti-inflammatory cytokines associated with the TLR4 pathway. Therefore, miR-451a may be partially responsible for immunomodulatory effects of adipose tissue-derived BiNPs.

scholarly journals Curcumin Ameliorates Chronic Mild Stress-Induced Depressive-Like Behavior via HMGB1/TLR4/NF-κB Signaling Pathway

2021 ◽  
Author(s):  
Li Miao ◽  
Fei Huang ◽  
Wei Jiang ◽  
Ying-ying Sun ◽  
Yong-jin Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Molecular Mechanisms ◽  
Immunofluorescent Staining ◽  
Antidepressant Effect ◽  
Therapeutic Drug ◽  
Inflammatory Disorder ◽  
Mild Stress ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4

Abstract BackgroundDepression, one of the most frequently-occurring psychiatric disorders worldwide, is a significant inflammatory disorder. The polyphenol curcumin (Cur), which is extracted from Curcuma longa, has marked anti-inflammatory and anti‑oxidative effects against inflammatory diseases. However, whether Cur has antidepressant effects and the possible mechanisms, are unclear. The present study aimed to assess Cur’s beneficial effects on depressive-like behaviors using a chronic unpredictable mild stress (CUMS) model and its possible molecular mechanisms. MethodsWe performed CUMS treated Sprague Dawley (SD) rats as a model of depression. Behavioral observations were performed by sucrose preference test (SPT), force swimming test (FST) and tail suspension test (TST). Hippocampal expression of oxidative stress markers and inflammatory cytokines were measured with ELISA. Hippocampal expression of high-mobility group box 1 (HMGB1), IL-1β, TNF-α and IL-6 were determined with quantitative PCR analyses and immunofluorescent staining. Hippocampal Toll-like receptor 4 (TLR4) and NF-κB activation were examined with Western blotting analysis.ResultsRats subjected to CUMS demonstrated marked depressive-like behavior (decreased locomotor activity and sucrose intake, and prolonged immobility). Their levels of oxidative stress and inflammatory cytokines increased significantly, and their levels of phosphorylated nuclear factor kappa-B (NF-κB), toll-like receptor 4 (TLR4), and HMGB1, also increased in the hippocampus. The changes were ameliorated significantly by treatment with Cur (50, 100 mg/kg) to varying degrees.Conclusion This study demonstrated that Cur has a potent antidepressant effect via the HMGB1/TLR4/NF-κB pathway, suggesting that Cur might be a promising therapeutic drug for depression.

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