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Terpenoids in Treatment of Liver Disease
Published in Dijendra Nath Roy, Terpenoids Against Human Diseases, 2019
Sujan Chatterjee, Debajyoti Patra, Pujita Ghosh, Akash Prasad, Kaustav Dutta Chowdhury
OA (3β-hydroxyolean-12-en-28-oic acid), a pentacyclic triterpenoid compound, is present in more than 146 families, 698 genera and 1,620 species of plants including many foodstuffs (e.g., Beta vulgaris L., virgin olive oils), fruits (e.g., apple, pomegranate, dates) and medicinal plants (e.g., Crataegus pinnatifida Bunge, Aralia chinensis, Eclipta alba) (Liu et al. 2013). Treatment of rats with OA (25 mg/kg per day, by gavage, once daily) over 10 weeks diminished fructose-induced excess hepatic TG accumulation without affecting total energy intake. Attenuation of the increased vacuolization was evident in the treated group. An hepatic gene expression profile demonstrated that OA-treatment suppressed fructose-stimulated overexpression of SREBP-1 and STREBP-1c mRNA. In accord, the overexpression of SREBP-1c–responsive genes responsible for fatty acid synthesis was also down-regulated, while overexpressed nuclear protein of carbohydrate response element-binding protein and its target genes like liver pyruvate kinase and microsomal TG transfer protein were not amended. Additionally, OA did not affect the expression of PPAR-γ and -α and their target genes. Modulation of hepatic SREBP-1c–mediated expression of the genes responsible for de novo fatty acid synthesis plays a pivotal role in OA-elicited diminishment of fructose-induced fatty liver in rats (Liu et al. 2013). OA pre-treatment also reduced the occurrence of liver injury by chemical exposure like bromobenzene, acetaminophen, phalloidin and cadmium. In addition, it is able to protect the liver from endotoxins like D-GalN and thioacetamide (Reisman et al. 2009; Jiménez-Arellanes et al. 2016).
Evaluation of sucrose-enriched diet consumption in the development of risk factors associated to type 2 diabetes, atherosclerosis and non-alcoholic fatty liver disease in a murine model
Published in International Journal of Environmental Health Research, 2021
Carolina Gabriela Plazas Guerrero, Selene De Jesús Acosta Cota, Francisco Humberto Castro Sánchez, Marcela De Jesús Vergara Jiménez, Efrén Rafael Ríos Burgueño, Juan Ignacio Sarmiento Sánchez, Lorenzo Antonio Picos Corrales, Ulises Osuna Martínez
In chronic hyperglycemic and hyperinsulinemic states, the levels and uptake of free fatty acids are higher, stimulating hepatic lipid synthesis and impairing β-oxidation (Ragab et al. 2015). This lipid synthesis, and as consequence its accumulation, is mainly due the stimulation of lipogenic pathways by insulin action that promotes the expression of Sterol regulatory element-binding protein-1 (SREBP-1) and carbohydrate responsive element-binding protein (ChREBP) in the liver, transcription factors involved in the expression of lipogenic genes, such as those involve in the synthesis of enzymes related with these pathways (Basciano et al. 2005; Pérez Cruz et al. 2007; Castro et al. 2014; Schultz et al. 2015).
Understanding the complex microenvironment in oral cancer: the contribution of the Faculty of Dentistry, University of Otago over the last 100 years
Published in Journal of the Royal Society of New Zealand, 2020
Alison Mary Rich, Haizal Mohd Hussaini, Benedict Seo, Rosnah Bt Zain
A further line of enquiry has been examining the effects of intrinsic and extrinsic stressful stimuli on the TME, specifically endoplasmic reticulum (ER) stress. ER stress leads to the activation of the unfolded protein response (UPR). This is an evolutionarily conserved set of mechanisms designed to ameliorate ER homeostatic imbalance or to induce cell death through apoptosis when ER stress cannot be mitigated. The UPR is extensively intertwined with other vital processes, including those that influence development and progression of cancer. As such, UPR has been implicated in either driving lesional dormancy or promotion and progression in multiple cancer types in a context-dependent manner, and it has been experimentally exploited as potential anti-cancer targets (Shen et al. 2018; Hsu et al. 2019). However, at this stage, the understanding of the role of ER stress-induced UPR in the pathogenesis and progression of OSCC is still in its infancy, requiring further elucidation. We undertook a series of investigations examining ER stress and the maintenance of OSCC cell viability and apoptosis and the differential regulation of key UPR and ER stress-associated genes in an established in-vitro model using the potent inducer of ER stress, tunicamycin. Seven extensively substantiated cell lines derived from normal, dysplastic and malignant oral keratinocytes were used. They were subjected to tunicamycin-induced ER stress of varying intensity and chronicity. In the cell viability experiments it was demonstrated that OSCC cells maintained cell viability in the presence of ER stress at a significantly greater level, compared to normal oral keratinocytes (Seo 2019). Furthermore, caspase-3/7 activity and DNA fragmentation, hallmarks of cell death, were suppressed in OSCC (Seo 2019) (Figure 7A,B). It was also discovered, for the first time, that UPR-induced apoptosis-related factors, most notably DNA damage inducible transcript (DDIT)-3, were significantly up-regulated in OSCC. Also, the master regulator of lipid metabolism, sterol regulatory binding factor (SREBP)-1, and CAMP responsive element binding protein 3-Like (CREB3L)-3, an ER-resident transcription factor closely related to activating transcription factor (ATF)-6, which plays an important role in linking ER stress with immune–inflammatory responses, were significantly up-regulated in OSCC (Seo 2019). These studies highlighted the importance of, and the influence of ER stress and UPR, on the pathogenesis and pathobiology of OSCC, especially centred around factors that influence apoptosis, TME and lipid metabolism.