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Garcinia indica (Kokum) and Ilex aquifolium (European Holly)
Published in Azamal Husen, Herbs, Shrubs, and Trees of Potential Medicinal Benefits, 2022
Dicson Sheeja Malar, Mani Iyer Prasanth, Tewin Tencomnao, James Michael Brimson, Anchalee Prasansuklab
UA acts as an activator of sterol regulatory element-binding protein 2 (SREBP2) to lower cholesterol in hepatocellular carcinoma cells and attenuates growth signaling pathways including ERK1/2, AKT, MEK to promote cell cycle arrest and apoptosis (Kim et al., 2019a). Further, UA blocks PI3/AKT, STAT-3 pathway to downregulate survivin leading to apoptosis (Tang et al., 2009; Liu et al., 2017). Moreover, dose-dependent AMPKα-mediated inhibition of DNMT1, whose overexpression results in hypermethylation and oncogenic activation is also observed upon treatment with UA (Yie et al., 2015). Exposure of UA to glioblastoma cells caused necrosis through the increased production of ROS, impairment of ATP level, and mitochondrial permeability transition pore opening (Lu et al., 2014). Further, proliferation of glioblastoma cells was inhibited by attenuating TGF-β1/miR-21/PDCD4 pathway and inducing JNK-dependent lysosomal associated cell death (Wang et al., 2012a; Conway et al., 2021). In addition, UA has been found to increase the chemosensitivity of cancer cells toward drugs in various resistant cancer cells (Lin et al., 2020; Li et al., 2020c; Chen et al., 2020a) indicating it can also be supplemented along with already existing anti-cancer drugs to improve their activity.
Healing the Heart with Whole Foods and Food Bioactives
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2015
From a nutrigenomic perspective, an animal study by Collison et al.149 demonstrated that an iTFA-containing diet induced over twice as many cardiac differentially expressed genes (DEGs) in males compared to females, including downregulation of Gata4, Mef2d, and Srebf2. This type of nutrigenomic research needs to be evaluated in human clinical trials as this information would be invaluable for making dietary recommendations and improving patient compliance to eating regimens.
Interaction effect between NAFLD severity and high carbohydrate diet on gut microbiome alteration and hepatic de novo lipogenesis
Published in Gut Microbes, 2022
Hyena Kang, Hyun Ju You, Giljae Lee, Seung Hyun Lee, Taekyeong Yoo, Murim Choi, Sae Kyung Joo, Jeong Hwan Park, Mee Soo Chang, Dong Hyeon Lee, Won Kim, GwangPyo Ko
The expression of SREBF2, the gene encoding sterol regulatory element-binding protein 2 (SREBP2), was upregulated upon increasing NAFLD severity in the HC group. SREBPs can activate the transcription of genes involved in the synthesis of cholesterol, fatty acids, and phospholipids.35,36 The association between SREBF2 and NASH is well established: SREBF2 mRNA levels are three times higher in NASH patients than in healthy controls, and acyl-CoA cholesterol acyltransferase was 1.5-fold increased.37 Thus, chronic carbohydrate consumption may stimulate SREBP expression and the subsequent upregulation of hepatic DNL, leading to excessive lipid accumulation and the onset of NAFLD. We also demonstrated that the diet-induced increase in hepatic SREBF2 expression was positively associated with the abundance of Enterobacteriaceae. Although a direct interaction between SREBP2 and Enterobacteriaceae has not yet been established, our results provide novel insights into the gut microbe mediation of DNL, which occurs via regulation of hepatic gene expression in relation to an HC diet.
Administration timing and duration-dependent effects of sesamin isomers on lipid metabolism in rats
Published in Chronobiology International, 2020
Norifumi Tateishi, Satoshi Morita, Izumi Yamazaki, Hitoshi Okumura, Masaru Kominami, Sota Akazawa, Ayuta Funaki, Namino Tomimori, Tomohiro Rogi, Hiroshi Shibata, Shigenobu Shibata
As shown in Figure 4a–c, SE decreased gene expression of Srebp2 and its downstream, transcriptional target molecules, Hmgcr and Ldlr. These results indicate that SE interacts with Srebp2 and might be important for the functional expression of SE’s effects on lipid metabolism. Thus, we performed a cell-based assay to assess whether sesamin and episesamin, compounds in SE, can modulate the functional activity of SREBP2. Data showed that sesamin and episesamin have antagonistic effects on SREBP2 (Figure 5a,b), with the effects being stronger in sesamin when compared to episesamin. In contrast, they have no agonistic effects on SREBP2 (data not shown). These data suggest that SE may inhibit SREBP2 function in its transcriptional (Figure 4b) and post-translational (Figure 5a,b) steps and these events may mediate the effects of timing of SE administration dependency on cholesterol metabolism.
Comparative omics analyses of hepatotoxicity induced by oral azole drugs in mice liver and primary hepatocytes
Published in Toxicology Mechanisms and Methods, 2019
Se-Myo Park, Seung-Jun Kang, Mi-Sun Choi, Soojin Kim, Seokjoo Yoon, Jung-Hwa Oh
In the comparison between in vitro and in vivo systems treated with KTZ, SREBFs were predicted to function as master regulators associated with hepatotoxicity induced by oral KTZ administration. SREBF1 and SREBF2 play key roles in cholesterol and fatty acid biosynthesis by compensatory regulation; they activate cell proliferation through activation of other transcription factors such as AhR and PPARA (Kawano et al. 2010). SREBF1/2 also induce cholesterol biosynthesis through cholesterol metabolism by P450 isotypes such as CYP7A1/CYP51A (Zhu et al. 2014). The results predicted that inhibition of cholesterol activates SREBF1/2 to induce cholesterol synthesis by positive feedback regulation. In addition, SREBF1/2 proteins induce inflammation or oxidative stress through tumor necrosis factor (TNF) and NFκB (Li et al. 2013).