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Anti-Obesity Potential of Indian Traditional Medicinal Plants and Their Phytochemicals
Published in Parimelazhagan Thangaraj, Medicinal Plants, 2018
Vellingiri Vadivel, Pichai Venkatalakshmi, Pemaiah Brindha
Platycodi radix, widely used in traditional oriental medicines as a remedy for respiratory disorders, is rich in saponins, which are responsible for a diversity of effects including anti-inflammation, anti-allergy, antitumor and immunostimulation (Zhao et al. 2010). Given its inhibitory action on pancreatic lipase (Xu et al. 2005), with platycodin-D as the most efficient compound (Zhan and Kim 2004), it ameliorated high fat-induced obesity in mice and rats (Zhao et al. 2010). SK1 is an edible saponin-rich compound from Platycodi radix that is able to reduce body weight and fat accumulation by increasing faecal lipid outputs in high-fat fed mice (Kim et al. 2009).
Arenaviruses and Neurovirology
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
GPC is posttranslationally cleaved into the G1 and G2 envelope proteins of the virus as well as a small (58-amino-acid) stable signal peptide (SSP) (Emonet et al. 2009). The cleavage is mediated by the SK1/S1P cellular protease (Kunz et al. 2003). It has been shown that the protease has a strong preference to arenaviral sequences resembling its autoprocessing sites. The Lassa fever virus resembles the protease C-site, whereas the Junin virus has a similarity to the B-site (Pasquato et al. 2011). The authors suggested that arenaviral GP complexes have evolved to mimic the protease’s autoprocessing sites to ensure efficient cleavage.
Travelers and workers at high altitude
Published in Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson, Ward, Milledge and West's High Altitude Medicine and Physiology, 2021
Andrew M. Luks, Philip N. Ainslie, Justin S. Lawley, Robert C. Roach, Tatum S. Simonson
Metabolomic profiles, which provide information on the metabolites within cells, tissues, or organisms, have also been characterized in individuals at sea level and high altitude. Sun et al. (2016) employed nonbiased high-throughput metabolomics for 21 volunteers taken from sea level to 5260 m and found that erythrocyte S1P, G-protein coupled receptor for the bioactive lysosphingolipid sphingosine 1-phosphate, increased and remained elevated for 16 days at high altitude and was correlated with increased erythrocyte sphingosine kinase 1 activity and hemoglobin oxygen release capacity. These results indicated a shift toward glycolysis when oxygen becomes scarce, which is consistent with other metabolomic studies of hypoxia performed in hypobaric chambers (Tissot van Patot et al. 2009). It has been further suggested that a “metabolic memory” persists beyond the initial exposure to hypoxia, as increased glycolysis remained for up to a week after returning to normoxia (d'Alessandro et al. 2016). Liu et al. (2016) showed that production of erythrocyte 2,3-bisphosphoglycerate (2,3-BPG), a negative allosteric regulator of hemoglobin-oxygen binding affinity, was induced by altitude, remained at increased levels for up to 16 days, and was associated with plasma adenosine concentrations and soluble CD73 activity. While these studies were based on limited sample sizes, the Caudwell Xtreme Everest study (Levett et al. 2010), with more than 200 individuals assessed periodically as they ascended from lowland to Everest base camp (5300 m), obtained both metabolomic and lipidomic information (O'Brien et al. 2019). They also identified metabolic shifts that pointed toward an increased glycolytic rate (i.e., decreasing isoleucine and glucose; increasing lactate) as well as fat-store mobilization (i.e., decreasing triglycerides; de novo lipogenesis; increasing levels of free fatty acids such as palmitic, linoleic, and oleic acids) with ascent. Overall, the studies to date support the notion that metabolic changes occur as early as within a few hours of ascending and have a cascade of downstream effects that can last up to a week or longer.
Molecular Targets of Curcumin and Its Therapeutic Potential for Ovarian Cancer
Published in Nutrition and Cancer, 2022
Malihe Mohamadian, Afsane Bahrami, Maryam Moradi Binabaj, Fereshteh Asgharzadeh, Gordon A. Ferns
Sphingosine kinase 1 (SphK1), a kinase that regulates the balance between ceramide/sphingosine and S1P amounts, controls cellular behaviors and may support tumor progression, including tumor formation, proliferation, metastasis, and invasion of malignant cells. SphK1 also is an important enzyme amplified within the neoplastic transformation. It has been demonstrated that SKI-II, an SphK1 inhibitor, combined with curcumin had a synergistic anti-cell proliferation impact in OC cell lines including SKOV3, CaOV3, and A2780. Moreover, curcumin-induced mitochondrial apoptosis pathways are facilitated by SKI-II which significantly increased curcumin-induced caspase-3 and PARP cleavage, as well as cytochrome c release. The results of the current study also showed that ceramide formation, p38 activation, and Akt inhibition mediated by curcumin are assisted in a synergistic way when SphK1 is inhibited via SKI-II. These findings imply that SKI-II potentiates curcumin-induced growth inhibition and apoptosis in OC cells (106).
HDL therapy today: from atherosclerosis, to stent compatibility to heart failure
Published in Annals of Medicine, 2019
C.R. Sirtori, M. Ruscica, L. Calabresi, G. Chiesa, R. Giovannoni, J.J. Badimon
A significant role of the sphingomyelin (SM) species, representing 5–10% in weight of total has been recognised in a number of recent reports. The SM derivative sphingosine-1-phosphate (S1P) in particular follows phosphorylation of cell membrane derived sphingosine through SphK1 (sphingosine kinase 1) and SphK2 (sphingosine kinase 2) [10]. S1P rapidly reaches high plasma concentrations being bound to albumin or HDL. This bioactive PL can influence the quality and quantity of HDL dependent function, particularly with the binding partner apolipoprotein M; ApoM deficient mice do not carry S1P and show a functional deficiency of HDL [11]. Cellular protection may be exerted also by way of opening of the mitochondrial channels, exerted by S1P, apo AI, clusterin and miRNA [12,13]. The mechanism appears to be that of induction of STAT3, subsequently bound by mitochondria, decreasing the permeability transition pore and preventing apoptosis [14].
Serum concentrations of aminoacylase 1 in schizophrenia as a potential biomarker: a case-sibling-control study
Published in Nordic Journal of Psychiatry, 2022
Diğdem Göverti, Rabia Nazik Yüksel, Hasan Kaya, Nihan Büyüklüoğlu, Çiğdem Yücel, Erol Göka
Aminoacylase 1 (ACY1; EC 3.5.1.14) is a homodimeric, cytosolic, zinc-metalloprotein, and endogenous mammalian enzyme that has a role in the catabolism of N-terminally acetylated proteins and amino acids by proteolytic degradation [5]. It hydrolyses N-acetylated derivates of methionine, glutamine, serine, alanine, glycine, leucine, and valine apart from N-acetyl-L-aspartate catalyzed by Aminoacylase 2 (EC 3.5.1.15) [6,7]. ACY1, also identified as a risk locus at schizophrenia and bipolar disorder, is encoded by chromosome 3p.21 and expressed by various tissue, particularly the brain and kidney [8,9]. Moreover, it regulates the function of the sphingosine kinase 1 enzyme defined with mitogenic and cytoprotective effects on cells [10].