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Coronary Artery Disease
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Another exciting genetic study on olive oil was performed by researchers in Spain.15 According to this study out of Cordoba, consuming olive oil high in phenols helps to reduce the expression of pro-inflammatory genes. For the 6-week trial, researchers recruited 20 men and women with metabolic syndrome, standardized their diets, and then had them consume an olive oil-based breakfast that was either high in phenols or low in phenols. After each meal, blood samples were analyzed. In total, 98 genes were identified as being affected by the amount of phenols the participants consumed. Most importantly, there was a reduction in pro-inflammatory genes associated with NF-kappaB. Since inflammation is the etiology of heart disease, a suppression of pro-inflammatory mediators with reversing genes back to a non-inflammatory state is indeed noteworthy. Olive oil may just be the ticket and is a simple intervention to protect yourself.
Brooke–Spiegler Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
By removing lys63-linked ubiquitin chains from several specific substrates, CYLD deubiquitinates several NF-kappa-B regulators (e.g., TRAF2, TRAF6, NEMO [IKBKG], and BCL3), and negatively regulates the nuclear factor-kappa B and c-Jun N-terminal kinase pathways [6]. Therefore, inhibition or loss of CYLD deubiquitinating activity enhances constitutive activation of transcription factor NF-kappa-B, increases resistance to apoptosis, and contributes to hyperproliferation and tumorigenesis. Indeed, reduced CYLD level induces B-cell lymphoma-3/p50/p52-dependent nuclear factor-κB activation and triggers the expression of genes encoding cyclin D1 and N-cadherin. In turn, elevated levels of cyclin D1 and N-cadherin promote melanoma proliferation and invasion [7,8].
Cardiovascular Disease and Oxidative Stress
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Marco Fernandes, Alisha Patel, Holger Husi
There is a strong association of obese patients developing type 2 diabetes mellitus (T2DM) (Eckel et al., 2011), thereby, secretion within the adipose tissue of free fatty acids (FFAs) and stimulatory cytokines directly impacts on insulin sensitivity (Kang et al., 2016) (Fig. 7.2). FFA-induced ROS production reduces activation of insulin receptor substrate 1 (IRS1) and the intracellular signal transduction PI3K-Akt pathway, and thereby leads to a reduction of the stimulus of the facilitated glucose transporter member 4 (SLC2A4/GLUT4) (Saltiel and Kahn, 2001). FFA-induces impairment of the PI3K-pathway, reduces Akt activity, and phosphorylation of endothelial NO synthase (eNOS), which in turn results in diminished production of NO, leading to endothelial dysfunction, and vascular remodelling (Fig. 7.2). Consequently, accumulation of ROS induces activation of the transcription factor NF-kappaB, which leads to CD14+ monocytes/macrophages increased release of pro-inflammatory adhesion molecules and cytokines (Wang Y. et al., 2011).
Ibuprofen and COVID-19 disease: separating the myths from facts
Published in Expert Review of Respiratory Medicine, 2021
Frideriki Poutoglidou, Athanasios Saitis, Dimitrios Kouvelas
As the ‘cytokine storm’ is mainly associated with the adverse outcomes in severe ill COVID-19 patients, the role of ibuprofen in the inflammatory process in SARS-CoV infection needs to be established. NF-kappa B is a transcription factor that, once activated, leads to the production of various cytokines and chemokines and is closely related with the ‘cytokine storm’ in COVID-19 disease [22]. It has been shown that ibuprofen can suppress NF-kappa B transcriptional activity [23]. At the same time, Interleukin-6 has been recognized as a key molecule in pulmonary inflammation and lung damage in patients with COVID-19 disease [24,25]. In addition, COVID-19 patients with moderate and severe disease may benefit from tocilizumab, an antibody against Interleukin-6 receptor (IL-6 R) [26]. Previous studies have shown that ibuprofen reduces the expression of Interleukin-6 [27,28]. An inhibition of Tumor Necrosis Factor-a and Interleukin-1β [29,30] has, also, been reported.
Resveratrol Combined with 17β-Estradiol Prevents IL-1β Induced Apoptosis in Human Nucleus Pulposus Via The PI3K/AKT/Mtor and PI3K/AKT/GSK-3β Pathway
Published in Journal of Investigative Surgery, 2021
Xiaoliang Bai, Xiaohui Guo, Feng Zhang, Long Zheng, Wenyuan Ding, Sidong Yang
Our lab has found that Resveratrol combined with 17β-estradiol can effectively inhibit the abnormal apoptosis of rat intervertebral disc cells, with the efficiency of anti-apoptosis better than that of 17β-estradiol or resveratrol alone [23]. Resveratrol together with 17β-estradiol may share the same receptor (estrogen receptor ER-a) [24], then fully utilize the related signal pathway to suppress IL-1β -mediated NP cell apoptosis. And it has been found that Resveratrol with 17β-estradiol promoted the PI3K/AKT signaling pathway to support the anti- apoptosis process [16]. PI3K/AKT is one of the most important pathways to modulate cell functions, downstream of which containing apoptosis-related proteins such as mTOR, GSK-3β, NF-kappaB and caspase-3 [25–28]. mTOR signaling pathway regulates cell growth by sensing changes in energy, oxygen concentration and pressure inside and outside cells [29]. Activated PI3K/AKT/mTOR signaling pathway can promote cell growth and protein synthesis, providing an anti-apoptotic basis for cells [30]. GSK-3β is a highly conserved and multifunctional serine/threonine kinase. It is one of the rate-limiting enzymes of glycogen synthase kinase. It is the substrate of AKT and participates in the regulation of cell death. NF-kappa B is an important transcriptional regulator in the nucleus and has a wide range of biological functions [31,32]. Activated NF-kappa B has both anti-apoptotic and pro-apoptotic effects, maybe dependent on the cell type, stimuli or other conditions.
The Effect of Intravenous Selenium on Oxidative Stress in Critically Ill Patients with Acute Respiratory Distress Syndrome
Published in Immunological Investigations, 2019
Ata Mahmoodpoor, Hadi Hamishehkar, Kamran Shadvar, Zohreh Ostadi, Sarvin Sanaie, Seied Hadi Saghaleini, Nader D. Nader
Attempts to decrease lung injury have focused on modulation of the signaling pathways leading to increased inflammatory cytokine production, and on restoration of the oxidant/antioxidant balance to limit the degree of oxidative cell damage. Moreover, several studies have shown that selenium at physiological levels inhibits activation of NF-kappa B transcription factor (Kwon et al., 2016; Maehira et al., 2003). As the transcription factor NF-kappa B is the final common step of the regulation for the expression of inflammatory cytokine, modulation of its activity has been the target of a number of anti-inflammatory drugs (Moine et al., 1997). In this study, despite a significant inverse correlation between the serum selenium concentrations and the serum levels of inflammatory markers (i.e., IL-1 beta IL-6), supplementation of selenium did not meaningfully add to downregulation of these cytokines in the plasma. Only the serum levels of IL-1 beta was somewhat lower in the selenium-treated group compared to the control on Day-7. This may indicate that only critically low levels of serum selenium may be responsible for over expression of the inflammatory response and additional supplementation of selenium does not meaningfully reduce this response despite a significant increase in antioxidant activity of GPx in the lungs.