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Herbal Therapies
Published in Anil K. Sharma, Raj K. Keservani, Surya Prakash Gautam, Herbal Product Development, 2020
H. Shahrul, M. L. Tan, A. H. Auni, S. R. Nur, S. M. N. Nurul
As a cardioprotective compound, Tan IIA had anti-atherosclerotic effect as it caused the reduction in the expression of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and CX3CL1. It inhibited the NF-κB signaling pathway in vascular endothelial cells (Chang et al., 2014). Treatment with Tanshinone IIA had significant inhibitory effect compared to S. miltiorrhiza extract alone on adhesion of monocytes to vascular endothelial cells. Besides, S. miltiorrhiza root extract also has antioxidant activity. Its hydrophilic components, protocatechuic aldehyde and Sal B could inhibit the TNF-α-induced expression of ICAM-1, VCAM-1, and the NF-κB and activator protein-1 DNA binding activities in human umbilical vein endothelial cells (Zhou et al., 2005). Adhesion molecules play a crucial function in the progression of atherogenesis. Endothelial cells produce the adhesion molecules after stimulation with various inflammatory cytokines.
Mathematical Modelling of Signalling Networks in Cancer
Published in Inna Kuperstein, Emmanuel Barillot, Computational Systems Biology Approaches in Cancer Research, 2019
Inna Kuperstein, Emmanuel Barillot
Here, we focus on the NF-κB signalling system, which is a pathway critically involved in the development of cancer but also cardiovascular and autoimmune diseases.6–8 The system comprises a canonical (or classical) pathway and a non-canonical (or alternative) pathway.9,10 Both signalling branches regulate transcription factors of the NF-κB family controlling a range of gene expression programs that affect inflammatory and immune responses as well as cell proliferation and cell death. In detail, the transcription factors bind the DNA as dimers, where the most common dimer related to the canonical pathway comprises p50 and RelA and the dimer related to the non-canonical pathway comprises p52 and RelB (Figure 4.2). A large number of stimuli can activate the NF-κB pathways regulating a network including receptors, adaptors, ligases and kinases that lead to the occurrence of active NF-κB dimers. The role of the NF-κB dynamics in regulating gene expression has been intensively studied.11,12
Mechanisms of Nanotoxicity to Cells, Animals, and Humans
Published in Vineet Kumar, Nandita Dasgupta, Shivendu Ranjan, Nanotoxicology, 2018
Belinda Wong Shu Ee, Puja Khanna, Ng Cheng Teng, Baeg Gyeong Hun
The NF-κB pathway is one of the well-studied inflammatory pathways that control DNA transcription, cytokine production, and cell survival. The NF-κB pathway becomes activated by PRRs and regulates cytokine production, contributing to inflammation (Arthur and Ley 2013). TLRs, bacterial products, and oxidative stress are other stimuli that can also activate this pathway (Giovanni et al. 2015). In the absence of a stimulus, NF-κB remains bound to the inhibitor of κB (IκB), thus is unable to translocate into the nucleus and promote the transcription of target genes. However, pro-inflammatory cytokines activate IκB kinase (IKK) complex composed of IKKα, IKKβ, and NF-κB essential modulator (NEMO), which then phosphorylates and degrades IκB. Degradation of IκB frees up NF-κB, which can now translocate into the nucleus and promote the expression of target genes (Arthur and Ley 2013). In vitro studies using RAW264.7 cells showed that an ultralow dosage of AgNPs, TiO2 NPs or ZnO NPs induces inflammatory response as evidenced by an increase in the expressions of NF-κB and pro-inflammatory genes such as IL-6, IL-1β, and TNF-α (Giovanni et al. 2015). In vivo studies using TiO2 NPs-exposed ICR mice exhibited neuro-inflammation via the NF-κB pathway, as proven by a dramatic increase in the expression of TLRs, TNF-α, and NF-κB (Ze et al. 2014).
The ROS/NF-κB/HK2 axis is involved in the arsenic-induced Warburg effect in human L-02 hepatocytes
Published in International Journal of Environmental Health Research, 2022
Fanshuo Yin, Ying Zhang, Xin Zhang, Meichen Zhang, Zaihong Zhang, Yunyi Yin, Haili Xu, Yanmei Yang, Yanhui Gao
It is known that arsenic at low concentrations contributes to cell proliferation and malignant transformation by activating certain signal pathways that are reported to be involved in regulating the Warburg effect (Presek et al. 1988; Medda et al. 2021). The nuclear factor kappa B (NF-κB) signaling pathway is one of these pathways (Xiong et al. 2020; Quiroga et al. 2021). This pathway, the most common dysfunctional signal pathway in human cancers, also plays a regulatory role in the Warburg effect by regulating the transcription of metabolic-related genes, such as hexokinase 2 (HK2) (Kooshki et al. 2021). NF-κB is a dimeric complex composed of five subunits, namely RelA (p65), RelB, c-Rel, NF-κB1 (p105/p50), and NF-κB2. The p65 subunit, as the main functional subunit, is involved in the function of the nuclear transcription factor (Hayden and Ghosh 2004, 2008). There is evidence that arsenic at low concentrations activates the NF-κB signaling pathway (Renu et al. 2020; Tang et al. 2021) and upregulates the HK2 protein, a key enzyme of glycolysis. It can therefore be hypothesized that the NF-κB signaling pathway may participate in the arsenic-induced Warburg effect by regulating the expression of HK2.
Potential protective roles of curcumin against cadmium-induced toxicity and oxidative stress
Published in Journal of Toxicology and Environmental Health, Part B, 2021
Jae Hyeon Park, Byung Mu Lee, Hyung Sik Kim
The role of natural products, such as those from plant seeds, flowers, leaves, and stems, is well known in the prevention of tumors. Curcumin suppresses the activity of drug-metabolizing enzymes cytochrome p450 reductase and cytochrome p450 (Rahmani et al. 2018). Based upon in vivo models Sharma et al. (2001) found that dietary curcumin upregulated the activity of phase II enzymes such as glutathione S-transferase (GST) while Wang et al. (2009) noted downregulation in the expression of vascular endothelial growth factor by inhibiting PPARδ in colon cancer cells. Jiang et al. (2015) also reported that curcumin-induced apoptosis and suppressed proliferation of melanoma cells. Activation of the NF-κB pathway is involved in carcinogenesis and required for tumor promotion and inflammation. Curcumin blocked cancer development by suppressing the promotion stage in carcinogenesis, since this compound inhibited the STAT3 and NF-κB signaling pathways. (Aggarwal et al. 2004; Marquardt et al. 2015; Philip, Rowley, and Schreiber 2004).
Inhibitory effect of particulate matter on toll-like receptor 9 stimulated dendritic cells by downregulating mitogen-activated protein kinase and NF-κB pathway
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Madeeha Arooj, Irshad Ali, Hee Kyoung Kang, Jin Won Hyun, Young-Sang Koh
Innate immune cells such as dendritic cells (DCs) and macrophages are key endogenous components to counteract pathogens and serve as a link between innate and adaptive immunity. Antigen-presenting cells (APCs) recognize pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs) (Akira and Takeda 2004; Koo et al. 2012). Toll-like receptors (TLRs) interaction with PAMPs activates major signal transduction pathways including mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and induces cytokine production which serves as a trigger to initiate T-cell-mediated immunity (Akira and Takeda 2004). MAPKs including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 kinase play a key role in apoptosis, cell survival, proliferation, differentiation, and inflammation. NF-κB is a rapid-acting transcription factor that aids in the expression of cytokines and cell survival. Under quiescent conditions, NF-κB, a transcription factor within cytosol is coupled with specific inhibitor nuclear factor of kappa light polypeptide gene enhancer in B-cells, alpha (IκBα). Upon TLR stimulation, IκBα is phosphorylated and ubiquitinated, which leads to proteasomal degradation and translocation of NF-κB into the nucleus where it regulates transcription of various inflammatory genes including cytokines (Akira and Takeda 2004; Blasius and Beutler 2010; Koo et al. 2012).