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Pharmaceutical Applications of Major Marine Nutraceuticals
Published in Se-Kwon Kim, Marine Biochemistry, 2023
P Madan Kumar, R Janani, S Priya, J Naveen, V Baskaran
In general, consuming high-calorie-rich diets and a sedentary lifestyle could result in obesity and diabetes mellitus. Excessive energy intake and accumulation of lipids in obesity can uplift the insulin resistance that leads to diabetes mellitus (Campfield et al., 1999). FUC has been shown to play an important role in reducing insulin resistance and elevated blood glucose levels. FUC administration to high-fat diet (HFD)–fed C57BL/6J mice resulted in significant reduction in blood glucose levels. However, FUC supplementation to C57BL/6J mice fed with normal chow diet did not affect the blood glucose levels, indicating the specificity of the blood glucose-lowering effect of FUC in diabetic conditions (Maeda et al., 2009; Hosokawa et al., 2010). TNF-α is involved in the development of type II diabetes, and its expression is positively correlated with insulin resistance (Hotamisligil et al., 1993). The administration of FUC (0.2%) to KK-mice significantly downregulated TNF-α mRNA levels and reduced the blood glucose and plasma insulin (Maeda et al., 2007). An FUC-rich diet ameliorated insulin resistance by promoting the expression of glucose transporter 4 mRNA in skeletal muscle tissues (Maeda et al., 2009).
The Human Immune System Seen from a Biomedical Engineering Viewpoint
Published in Robert B. Northrop, Endogenous and Exogenous Regulation and Control of Physiological Systems, 2020
TNFα, or cachectin, is a 17-kDa soluble protein trimer. It is the product of activated macrophages, fibroblasts, mast cells, and some T- and NK cells. Peritoneal mast cells have preformed, reserve TNFα available for immediate release upon appropriate stimulation. TNFα can induce fever, either by stimulating the release of pyrogenic prostaglandins or by causing the release of IL1, which is also pyrogenic. TNFα plays a major positive role in fighting local infections. It induces the production of acute-phase proteins, mobilizes neutrophils, activates T- and B-cells, increases the release of antibodies and complement, increases the adhesion of platelets to blood vessel walls, and increases the extravasation of lymphocytes and macrophages (diapedesis) to fight the infection in intracellular space. These actions result in the phagocytosis of the pathogens, local vessel occlusion, and the drainage of cells, debris, and fluid into the lymphatic system. These actions, carried out with other relevant cytokines, lead to the removal of the infecting pathogen and eventual tissue repair. TNFα also can bind to TNF receptors on tumor cells and kill them. Some tumor cells shed their TNF receptors, which become soluble and bind to TNFa, inactivating it. Excess TNFα can also lead to the body creating antibodies to it, giving similar deactivation. The mechanism of infected cell killing by TNFα is not known.
The Role of Nanoparticles in Cancer Therapy through Apoptosis Induction
Published in Hala Gali-Muhtasib, Racha Chouaib, Nanoparticle Drug Delivery Systems for Cancer Treatment, 2020
Marveh Rahmati, Saeid Amanpour, Hadiseh Mohammadpour
TNFα is induced by cytokines which are released by inflammatory cells and particularly activated macrophages. TNFα is the main extrinsic stimulus of extrinsic apoptosis. TNFR1 and TNFR2 are two receptors for TNFα in most cells. After the binding of TNFα to TNFR1, CASP-8 is activated in DICS complex, which contains the intermediate membrane proteins TNF receptor-associated death domain (TRADD). TRADD subsequently recruits other effector proteins such as FADD/MORT1 (FAS-Associated Death Domain Protein) into DISC complex. Regardless of apoptosis, the TNFα-TNFR pathway can also indirectly activate some of the transcription factors involved in cell survival and inflammatory responses [34]. In response to TNF induction, the transcription factor NF-κB and MAP kinases, including ERK, p38, and JNK, are activated in most cell types. Apoptosis or necrosis could also be initiated.
Implications of toxicity testing for health risk assessment of vapor-phase and PM2.5-bound polycyclic aromatic hydrocarbons during the diesel engine combustion
Published in Human and Ecological Risk Assessment: An International Journal, 2022
Guan-Fu Chen, Ying-Chi Lin, Yuan-Chung Lin, Chia-Chi Wang, Wei-Hsiang Chen
The immunotoxicity of samples was determined by a pro-inflammatory cytokine of TNF-alpha which is critical in immune cell homeostasis and pathophysiology. TNF-alpha modulates different toxic endpoints associated with exposure to PAHs (Kabatkova et al. 2015). TNF-alpha was released from stimulated monocyte/macrophages and is important in the initial stage of inflammation in tissue injury. The increase of TNF-alpha can give rise to inflammatory pathological responses. These responses included asthma, bronchitis, obstructive pulmonary disease, respiratory distress syndrome, and acute lung injury (Mukhopadhyay et al. 2006). In our study, human monocyte THP-1 cells (5 × 105 cells/mL) were cultured with the RPMI 1640 medium in 48-well plates (Wang et al. 2011). Different concentrations of sample extracts and lipopolysaccharide (LPS; 0.5 μg/mL) used as a loading control were added to each well. The cells were incubated in a chamber environment of 5% CO2 at 37 °C. After the 48-h contact time, the supernatants were collected and analyzed for the TNF-alpha concentration by using the standard sandwich ELISA described previously. The TNF-alpha concentration indicating the pro-inflammatory responses of cells exposed to different samples was calculated by dividing the TNF-alpha of the sample by the TNF-alpha of lipopolysaccharide. A result exceeding or below 100% represents a response of induction or inhibition, respectively (Wang et al. 2016a).
Effects of tumor necrosis factor (TNF) gene polymorphisms on the association between smoking and lung function among workers in swine operations
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Zhiwei Gao, James A. Dosman, Donna C. Rennie, David A. Schwartz, Ivana V. Yang, Jeremy Beach, Ambikaipakan Senthilselvan
Tumor necrosis factor-α (TNF-α) is an important pro-inflammatory cytokine and plays a critical role in combating infection and expression of many important chemokines and cytokines. TNF-α has been associated with many inflammatory or autoimmune diseases including asthma, chronic bronchitis, and COPD (Demirjian et al. 2006; May, Romberger, and Poole 2012; Mukhopadhyay, Hoidal, and Mukherjee 2006). Several studies demonstrated that polymorphisms in the tumor necrosis factor (TNF) gene are associated with asthma, atopic asthma, and serum IgE levels (Migita et al. 2005; Noguchi et al. 2002; Sharma et al. 2006). Specifically, polymorphisms in the promoter region of the TNF gene were noted to play a regulatory role in the production of TNF-α in response to different stimuli (Higuchi et al. 1998; Lv et al. 2006; Puthothu et al. 2009) and significantly associated with lung function decline among grain workers exposed to grain dust (Pahwa et al. 2009b). McDuffie et al. (2006) reported that promoter region polymorphisms of rs1800629 in the TNF gene significantly altered the adverse risk of cigarette smoking on lung function (percent of predicted FEV1 and FVC) among male grain workers. However, little information is available regarding whether promoter polymorphisms in the TNF gene might influence the impact of smoking on lung functions among workers in swine operations. Thus, this study aimed to examine whether promoter polymorphisms in the TNF gene might significantly modify the risk of reduced lung function associated with smoking among workers in swine operations.
Expression levels of selected cytokines and microRNAs in response to vitamin D supplementation in ultra-marathon runners
Published in European Journal of Sport Science, 2020
D. Pastuszak-Lewandoska, D. Domańska-Senderowska, J. Kiszałkiewicz, P. Szmigielska, A. Snochowska, W. Ratkowski, M. Spieszny, T. Klocek, P. Godlewski, P. Cięszczyk, E. Brzeziańska-Lasota, A. V. September, M. J. Laguette
As a prototypical pro-inflammatory cytokine, TNF-α is involved in inflammation and the acute-phase response. As the second measurement of relative abundance was done 12 h after the UM, the TNF-α mRNA response in this study could be associated with the progression of recovery from overtraining (Joro, Uusitalo, DeRuisseau, & Atalay, 2017) but should be interpreted with caution because of the high inter-individual variability. In other studies performed in marathon runners, increased TNF-α levels were observed after a race, while the level of TNF-α mRNA was not measured (Gill et al., 2015; Ostrowski et al., 1998) or the differences were not significant (Bernecker et al., 2013).