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Naturally Occurring Histone Deacetylase (HDAC) Inhibitors in the Treatment of Cancers
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Sujatha Puttalingaiah, Murthy V. Greeshma, Mahadevaswamy G. Kuruburu, Venugopal R. Bovilla, SubbaRao V. Madhunapantula
Recent studies have shown that HDACis have the potential of modulating immune functions as they were involved in controlling the NF-κB and STAT3 pathways (Dickinson et al., 2010; Schotterl et al., 2015). NF-κB plays a critical role in the innate and adaptive immune responses, cell proliferation, inhibition of apoptosis, promotion of cell migration, invasion and stimulation of angiogenesis and metastasis, which lead to the acceleration of cancer progression (Grivennikov et al., 2010).
Immunomodulatory Effect of Plant-Based Extracts on Neurodegeneration
Published in P. Mereena Luke, K. R. Dhanya, Didier Rouxel, Nandakumar Kalarikkal, Sabu Thomas, Advanced Studies in Experimental and Clinical Medicine, 2021
Koel Sinha, Chitrangada Das Mukhopadhyay
ALS, another neurodegenerative disease has got a beneficial effect of WS. The misfolded aggregation of TAR DNA binding protein-43 (TDP-43) is the main feature of ALS pathology. TDP-43 generally binds and coactivates the P-65 subunit of nuclear factor kappa beta (NF-κB). This NF-κB acts as a vital factor in disease pathology. On administration of the potent bioactive constituent withaferin-A in transgenic mouse model showed a marked improvement in ALS pathology whereas, this withaferin-A acts as an antagonist to NF-κB showed a remarkable reduction in the inflammatory response in the transgenic mice model [48]. Other observations suggested a marked improvement in ALS mice model by administration of withaferin-A which delayed the disease onset and progression. Later on, the root extract of WS with human TDP-43 mutation showed clearance of abnormal TDP-43 in neurons and showed improvement in motor as well as cognitive functions. Therefore, this adverse situation can be overcome by the administration of WS extract on neurodegenerative patients.
Nuclear Factor Kappa-B: Bridging Inflammation and Cancer
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Mohammad Aslam Khan, Girijesh Kumar Patel, Haseeb Zubair, Nikhil Tyagi, Shafquat Azim, Seema Singh, Aamir Ahmad, Ajay Pratap Singh
NF-κB transcriptionally regulates expression of genes which are involved in cell survival, apoptosis, differentiation and immune responses [42, 43]. As discussed above, NF-κB family consists of five members. Both the precursors (NF-κB1/p105 and NF-κB2/ p100) contain IκB-homologous regions at the C-terminal that function as NF-κB inhibitors. Proteolytic processing removes inhibitory domains, allowing the processed proteins (NF-κB1/ p50 and NF-κB2/p52) to enter into the nucleus. Inside the nucleus, p50 and p52 form homodimers or heterodimers with Rel family proteins [42]. All these NF-κB associated proteins have Rel homology domain (RHD) at the N-terminal region. Some of the NF-κB proteins (p65, c-Rel and RelB) contain transcriptional activation domain (TAD) at C-terminal, and these TAD containing proteins positively regulate transcriptional activity. On the other hand, two TAD lacking proteins, p52 and p100, negatively regulate gene expression when bound as homodimer, but can activate gene expression when recruited with other TAD containing proteins like p65. RelB and cRel [44]. Activation of NF-κB pathway is either by classical/canonical or the alternate/non-canonical signaling pathways.
Phytochemicals with protective effects against acute pancreatitis: a review of recent literature
Published in Pharmaceutical Biology, 2022
Yao Tang, Mingli Sun, Zhenning Liu
The transcription factor NF-κB is an important nuclear factor that plays a variety of evolutionarily conserved roles in a plethora of cellular and biological processes. NF-κB affects many cellular responses including inflammation, apoptosis and proliferation by regulating target gene expression. During the development of AP, NF-κB is activated rapidly in pancreatic acinar cells, and then multiple inflammatory cytokines (TNF, IL-6 and IL-1β) and chemokines (MCP-1 and MIP-1α) are significantly increased which can affect vascular permeability and contribute to thrombosis, haemorrhage and tissue necrosis (Steinle et al. 1999). Substantial evidence indicates NF-κB activation to be a key event in the progression of AP (Jakkampudi et al. 2016); therefore, inhibition of NF-κB activation and proinflammatory cytokines release may be a good therapeutic strategy for the attenuation of AP.
(E)-5-hydroxy-7-methoxy-3-(2′-hydroxybenzyl)-4-chromanone isolated from Portulaca oleracea L. suppresses LPS-induced inflammation in RAW 264.7 macrophages by downregulating inflammatory factors
Published in Immunopharmacology and Immunotoxicology, 2021
Eunji Kang, Jae Eun Park, Youngwan Seo, Ji Sook Han
Expression of inflammatory cytokines is regulated by the NF-κB transcription factor [17]. NF-κB is a transcription factor that regulates intracellular synthesis of various mediators such as cytokines and chemokines. NF-κB is released from IκB when IκB is phosphorylated by a stimulator such as LPS. It migrates to the nucleus and induces the synthesis of various mediators such as iNOS, COX-2 and inflammatory cytokines [18]. Thus, the inhibitory effect of HM-chromanone on IκB phosphorylation and NF-κB activation was investigated in LPS-stimulated RAW 264.7 cells. As a result, the phosphorylation of IκB was increased by LPS stimulation, and on the contrary, the phosphorylation of IκB was decreased by HM-chromanone, confirming that phosphorylation of IκB was inhibited (Figure 5). When the phosphorylation of IκB occurs, NF-κB bound to IκB is liberated and its migration into the nucleus increases. However, HM-chromanone significantly reduced nuclear translocation of NF-κB and also downregulated the expression of NF-κB. Immunofluorescence staining (Figure 6) shows that LPS stimulation caused obvious translocation of NF-kB p65 from cytoplasm into nucleus, which was counteracted obviously by pretreatment of HM-chromanone.
Glycyrrhizin improves bone metabolism in ovariectomized mice via inactivating NF-κB signaling
Published in Climacteric, 2021
Y. Tang, X. L. Lv, Y. Z. Bao, J. R. Wang
Glycyrrhizin is the most medically efficacious component of the licorice plant, with strong antivirus, anti-inflammatory, antioxidant, and antitumor properties. Several research studies have revealed protective functions of glycyrrhizin in diseases including virus infection, metabolic disorders, alcoholic liver injury, autoimmune encephalomyelitis, and so on13–17. A previous study reports that glycyrrhizin inhibits RANKL-induced osteoclastogenesis and reduces oxidative stress in bone marrow-derived monocytes (BMMs)18. A later study reveals that glycyrrhizin attenuates osteoclast formation and preserves bone mass and trabecular structure in OVX mice19, implying that glycyrrhizin would become a promising adjuvant therapeutic for PMO. However, the mechanism involved in the anti-osteoporosis effect of glycyrrhizin in vivo is unknown. In the present study, we explore the underlying mechanisms by mainly focusing on the NF-κB signaling pathway in vivo.