Tumor necrosis factor alpha has a crucial role in increased reactive oxygen species production in platelets of mice injected with lipopolysaccharide

Naime, Ana Carolina Antunes; Bonfitto, Pedro Henrique Leite; Solon, Carolina; Lopes-Pires, Maria Elisa; Anhê, Gabriel Forato; Antunes, Edson; Marcondes, Sisi

doi:10.1080/09537104.2019.1588241

Cited by 18 publications

(17 citation statements)

References 33 publications

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“…In return, a persistent decrease in cochlear microcirculation will again cause a persistent decrease in partial oxygen pressure, as both parameters are closely related 14 . Persistent decreases in partial oxygen pressure cause formation of reactive oxygen species, 31 which in turn cause activation of TNF pathways, 40 creating a vicious cycle (Figure 4). This view is further supported by the fact that TNF may cause cochlear inflammation in concentrations that are not sufficient to directly cause apoptosis of hair cells, yet is still able to cause shifts in hearing thresholds 41 …”

Section: Discussion/conclusionmentioning

confidence: 99%

Lipopolysaccharide decreases cochlear blood flow dose dependently in a guinea pig animal model via TNF signaling

et al. 2021

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Acute otitis media is one of the most common infectious diseases, affecting up to 11% of the worldwide population, reflecting between 300 and 700 million patients per year. 1 About half the patients affected are children, 1 and otitis media (including its chronic forms) is responsible for up to 3.200 deaths per year. 2 About 140 million patients retain a hearing impairment after acute otitis media each year, which can be caused by persisting perforation of the tympanic membrane or suppurative labyrinthitis and subsequent sensorineural hearing loss. 3

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Section: Discussion/conclusionmentioning

confidence: 99%

Lipopolysaccharide decreases cochlear blood flow dose dependently in a guinea pig animal model via TNF signaling

et al. 2021

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“…Its production is generally the combination of some stimulating factors such as LPS and specific receptors of monocytes or macrophages. [ 74 ] These stimulating factors activate transcription factors through a series of signal transduction and initiate downstream TNF gene transcription. [ 75 ] IL6 gene encodes a cytokine that functions in inflammation and the maturation of B cells.…”

Section: Discussionmentioning

confidence: 99%

Investigation on the mechanisms of guiqi huoxue capsule for treating cervical spondylosis based on network pharmacology and molecular docking

et al. 2021

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Background: Guiqi huoxue capsule (GQHXC) is a patented Chinese medicine used for treating a liver and kidney deficiency and blood stasis syndrome due to qi deficiency. It is caused by cervical spondylosis (cervical spondylotic radiculopathy (CSR), mixed cervical spondylosis mainly composed of nerve root type). Its underlying mechanisms need, however, to be further clarified. Methods: In this study, collecting compounds, predicting therapeutic targets, constructing networks, and analyzing biological functions and pathways were based on network pharmacology analysis. In addition, molecular docking verification was engaged to assess the binding potential of selected target-compound pairs. Results: We established 5 networks: compound-putative target network of GQHXC, protein-protein interaction (PPI) network related to CSR, compound-CSR target network, potential therapeutic targets PPI network, and herb-compound-target-pathway network. Network analysis indicated that 7 targets (tumor necrosis factor [TNF], interleukin 6 [IL6], nitric oxide synthase 3 [NOS3], Interleukin-8 [CXCL8], prostaglandin-endoperoxide synthase 2 [PTGS2], vascular endothelial growth factor A [VEGFA], and AP-1 transcription factor subunit [JUN]) might be the therapeutic targets of GQHXC in CSR. Moreover, molecular docking verification showed that TNF, IL6, NOS3, CXCL8, PTGS2, VEGFA, and JUN had a good is interaction with the corresponding compounds. Furthermore, enrichment analysis indicated that GQHXC might exert a curative role in CSR by regulating some important pathways, such as TNF signaling pathway, NF–kappa B signaling pathway, AGE–RAGE signaling pathway in diabetic complications, and so on. Conclusion: Our study preliminarily explained the underlying mechanisms of GQHXC for treating CSR, and molecular docking verification was adopted as an additional verification. These findings laid a valuable foundation for experimental research and further application of GQHXC in the clinical treatment of CSR.

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“…It has been shown that in diabetes and obesity as well as in spleen or kidney failure and CNS diseases, as a result of low reactivity of platelet receptors, their dysfunction occurs, which leads, among others, to blood clotting disorders ( 8 , 20 , 76 , 80 ), causing blood vessel embolism ( 16 , 22 , 76 , 92 , 108 ) and thrombosis ( 10 , 11 , 20 , 30 , 42 , 62 , 64 , 76 , 80 , 99 , 109 ). The role of platelets has also been demonstrated in myocardial infarction, because the change in their activation mediated by PAR-1 and P2Y12 receptors in terms of, e.g., aggregation, leads to increased blood clotting and the formation of a thrombus composed mainly of fibrin, platelets and a large amount of vWF ( 19 , 46 , 85 , 110 – 112 ). This causes coronary occlusion and may lead to atheromatous plaque rupture and inflammation.…”

Section: Platelets and Inflammationmentioning

confidence: 99%

“…aureus , PMPs and kinocidins present in the phagocytic vacuole degrade these bacteria ( 43 ). This pathway of direct neutralisation of bacteria by platelets also includes the interaction with platelets based on their ability to migrate, adhere, absorb, and also intracellularly kill as a result of the production of ROS reactive oxygen species ( 8 , 10 , 11 , 17 , 21 , 23 – 25 , 34 , 37 , 41 , 42 , 48 , 58 , 59 , 78 , 100 , 110 , 121 – 124 ). This direct destructive effect of platelets on bacteria, separately caused by migration, adherence and absorption of platelets, was recorded during infection with Bacillus sp.…”

Section: Platelets and Bacterial Infectionsmentioning

confidence: 99%

What Function Do Platelets Play in Inflammation and Bacterial and Viral Infections?

et al. 2021

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The article presents the function of platelets in inflammation as well as in bacterial and viral infections, which are the result of their reaction with the endovascular environment, including cells of damaged vascular endothelium and cells of the immune system. This role of platelets is conditioned by biologically active substances present in their granules and in their specific structures – EV (extracellular vesicles).

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Tumor necrosis factor alpha has a crucial role in increased reactive oxygen species production in platelets of mice injected with lipopolysaccharide

Cited by 18 publications

References 33 publications

Lipopolysaccharide decreases cochlear blood flow dose dependently in a guinea pig animal model via TNF signaling

Lipopolysaccharide decreases cochlear blood flow dose dependently in a guinea pig animal model via TNF signaling

Investigation on the mechanisms of guiqi huoxue capsule for treating cervical spondylosis based on network pharmacology and molecular docking

What Function Do Platelets Play in Inflammation and Bacterial and Viral Infections?

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