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Natasa Poklar Ulrih - One of the best experts on this subject based on the ideXlab platform.
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sitosterol and Gentisic Acid loaded 1 2 dipalmitoyl sn glycero 3 phosphocholine liposomal particles
JOURNAL OF ENGINEERING & PROCESSING MANAGEMENT, 2020Co-Authors: Aleksandra Jovanovic, Bojana D Balanc, Ajda Ota, Verica Djordjevic, Katarina Savikin, Viktor Nedovic, Natasa Poklar UlrihAbstract:The aim of the present study was the examination of the impact of -sitosterol andGentisic Acid on the characteristics of 1,2-dipalmitoyl-sn-glycero-3-phosphocholine(DPPC) liposomal particles: (a) bilayer permeability (fluorescence spectroscopy),(b) particle size, polydispersity index (PDI) and zeta potential (photon correlationspectroscopy) and (c) thermal properties (differential scanning calorimetry). -sitosterol induced the increase of liposomal bilayer rigidity, due to rearranging ofthe phospholipid chains, while Gentisic Acid enhanced the membrane fluidity, dueto the reduced orderliness and the increase of phospholipid dynamics. The inclusionof -sitosterol in liposomes caused a significant increase in particle diameterand PDI, while the encapsulation of Gentisic Acid did not have influence on particlesize distribution. Apart from that, the presence of -sitosterol resulted in thesignificant zeta potential increase, and thus a better stability of liposomal spheres(in the absence and in the presence of Gentisic Acid). -sitosterol decreased maintransition temperature (Tm) and phase transition enthalpy (H), and caused thedisappearance of the pre-transition peak as well, whereas the presence of GentisicAcid produced a slight decrease in Tm and increase of H. Therefore, Gentisic Acidhad more favourable, stabilizing interactions with phospholipids than -sitosterol.Thus, it can be concluded that -sitosterol is located in the bilayer interior betweenphospholipids acyl chains, and Gentisic Acid is incorporated near the outer leaflet ofthe phospholipid membrane, next to the polar head groups. -sitosterol and GentisicAcid loaded DPPC liposomal particles have a potential to be used in food andpharmaceutical products, due to the important individual and possible synergisticbeneficial health properties of -sitosterol and Gentisic Acid.
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effect of Gentisic Acid on the structural functional properties of liposomes incorporating β sitosterol
Colloids and Surfaces B: Biointerfaces, 2019Co-Authors: Aleksandra Jovanovic, Bojana D Balanc, Ajda Ota, Verica Djordjevic, Katarina Savikin, Viktor Nedovic, Mihaela Skrt, Branko Bugarski, Natasa Poklar UlrihAbstract:Abstract Multifunctional liposomes incorporating β-sitosterol were developed for delivery of Gentisic Acid (GA). The interactions of both compounds with phospholipid bilayer were interpreted viaeffects of different β-sitosterol content (0, 20 and 50 mol %) and different Gentisic Acid to lipid ratio (nGA/nlip from 10-5 to 1) on membrane fluidity and thermotropic properties. Multilamellar vesicles of phosphatidylcholines (with size range between 1350 and 1900 nm) effectively encapsulated GA (54%) when nGA/nlip was higher than 0.01. Suppression of lipid peroxidation was directly related to concentration of GA. The resistance to diffusion of Gentisic Acid from liposomes increased for ˜50% in samples incorporating 50 mol % β-sitosterol compared to sterol-free liposomes. Finally, simulated in vitro gastrointestinal conditions showed that the release was mainly affected by low pH of simulated gastric fluid and the presence of cholates in simulated intestinal fluid, rather than by enzymes activity.
Myung Ho Jeong - One of the best experts on this subject based on the ideXlab platform.
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Gentisic Acid prevents the transition from pressure overload-induced cardiac hypertrophy to heart failure
Nature Publishing Group, 2019Co-Authors: Simei Sun, Hae Jin Kee, Yuhee Ryu, Sin Young Choi, Gwi Ran Kim, Hyung-seok Kim, Seung-jung Kee, Myung Ho JeongAbstract:Abstract We previously reported that Gentisic Acid attenuates cardiac hypertrophy and fibrosis in transverse aortic constriction (TAC)-induced cardiac hypertrophy. Here, we examined whether Gentisic Acid prevents the development of heart failure. Heart failure was induced in mice via chronic TAC. Mice were administered the vehicle, Gentisic Acid (10 and 100 mg∙kg−1∙day−1), or bisoprolol (0.5 mg∙kg−1∙day−1) orally for 3 weeks, beginning 3 weeks after TAC. After oral administration of Gentisic Acid (2000 mg∙kg−1), no significant differences in organ weight, histology, or analyzed serum and hematological parameters were observed between female mice in the control and Gentisic Acid-treated groups. Gentisic Acid administration inhibited cardiac dysfunction in a dose-dependent manner, and reduced cardiac hypertrophy and fibrosis, as was revealed via western blotting, quantitative real-time PCR, and Masson’s trichrome staining. Gentisic Acid dose-dependently reduced the expression of fibrosis marker genes, suppressed the renin-angiotensin-aldosterone system, and reduced lung size and pulmonary vascular remodeling. Our data indicate that Gentisic Acid prevents cardiac hypertrophy, fibrosis, cardiac dysfunction, and pulmonary pathology in TAC-induced heart failure. These findings suggest that supplementation with Gentisic Acid may provide an advantage in preventing the progression from cardiac hypertrophy to heart failure
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Gentisic Acid attenuates pressure overload induced cardiac hypertrophy and fibrosis in mice through inhibition of the erk1 2 pathway
Journal of Cellular and Molecular Medicine, 2018Co-Authors: Simei Sun, Hae Jin Kee, Yuhee Ryu, Sin Young Choi, Gwi Ran Kim, Li Jin, Myung Ho JeongAbstract:We previously reported that Gentisic Acid (2,5-dihydroxybenzoic Acid) is the third most abundant phenolic component of Dendropanax morbifera branch extracts. Here, we investigated its effects on cardiac hypertrophy and fibrosis in a mouse model of pressure overload and compared them to those of the beta blocker bisoprolol and calcium channel blocker diltiazem. Cardiac hypertrophy was induced in mice by transverse aortic constriction (TAC). Beginning 2 weeks after this procedure, the mice were given daily intraperitoneal injections of Gentisic Acid (100 mg/kg/d), bisoprolol (5 mg/kg/d) or diltiazem (10 mg/kg/d) for 3 weeks. Cardiac hypertrophy was evaluated by the heart weight-to-body weight ratio, the cardiomyocyte cross-sectional area after haematoxylin and eosin staining, and echocardiography. Markers of cardiac hypertrophy and fibrosis were tested by reverse transcription-quantitative real-time polymerase chain reaction, western blotting and Masson's trichrome staining. The suppressive effects of Gentisic Acid treatment on TAC-induced cardiac hypertrophy and fibrosis were comparable to those of bisoprolol administration. Cardiac hypertrophy was reversed and left ventricular septum and posterior wall thickness were restored by Gentisic Acid, bisoprolol and diltiazem treatment. Cardiac hypertrophic marker gene expression and atrial and brain natriuretic peptide levels were decreased by Gentisic Acid and bisoprolol, as were cardiac (interstitial and perivascular) fibrosis and fibrosis-related gene expression. Cardiac hypertrophy-associated upregulation of the transcription factors GATA4 and Sp1 and activation of extracellular signal-regulated kinase 1/2 were also negated by these drugs. These results suggest that Gentisic Acid could serve as a therapeutic agent for cardiac hypertrophy and fibrosis.
Aleksandra Jovanovic - One of the best experts on this subject based on the ideXlab platform.
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sitosterol and Gentisic Acid loaded 1 2 dipalmitoyl sn glycero 3 phosphocholine liposomal particles
JOURNAL OF ENGINEERING & PROCESSING MANAGEMENT, 2020Co-Authors: Aleksandra Jovanovic, Bojana D Balanc, Ajda Ota, Verica Djordjevic, Katarina Savikin, Viktor Nedovic, Natasa Poklar UlrihAbstract:The aim of the present study was the examination of the impact of -sitosterol andGentisic Acid on the characteristics of 1,2-dipalmitoyl-sn-glycero-3-phosphocholine(DPPC) liposomal particles: (a) bilayer permeability (fluorescence spectroscopy),(b) particle size, polydispersity index (PDI) and zeta potential (photon correlationspectroscopy) and (c) thermal properties (differential scanning calorimetry). -sitosterol induced the increase of liposomal bilayer rigidity, due to rearranging ofthe phospholipid chains, while Gentisic Acid enhanced the membrane fluidity, dueto the reduced orderliness and the increase of phospholipid dynamics. The inclusionof -sitosterol in liposomes caused a significant increase in particle diameterand PDI, while the encapsulation of Gentisic Acid did not have influence on particlesize distribution. Apart from that, the presence of -sitosterol resulted in thesignificant zeta potential increase, and thus a better stability of liposomal spheres(in the absence and in the presence of Gentisic Acid). -sitosterol decreased maintransition temperature (Tm) and phase transition enthalpy (H), and caused thedisappearance of the pre-transition peak as well, whereas the presence of GentisicAcid produced a slight decrease in Tm and increase of H. Therefore, Gentisic Acidhad more favourable, stabilizing interactions with phospholipids than -sitosterol.Thus, it can be concluded that -sitosterol is located in the bilayer interior betweenphospholipids acyl chains, and Gentisic Acid is incorporated near the outer leaflet ofthe phospholipid membrane, next to the polar head groups. -sitosterol and GentisicAcid loaded DPPC liposomal particles have a potential to be used in food andpharmaceutical products, due to the important individual and possible synergisticbeneficial health properties of -sitosterol and Gentisic Acid.
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effect of Gentisic Acid on the structural functional properties of liposomes incorporating β sitosterol
Colloids and Surfaces B: Biointerfaces, 2019Co-Authors: Aleksandra Jovanovic, Bojana D Balanc, Ajda Ota, Verica Djordjevic, Katarina Savikin, Viktor Nedovic, Mihaela Skrt, Branko Bugarski, Natasa Poklar UlrihAbstract:Abstract Multifunctional liposomes incorporating β-sitosterol were developed for delivery of Gentisic Acid (GA). The interactions of both compounds with phospholipid bilayer were interpreted viaeffects of different β-sitosterol content (0, 20 and 50 mol %) and different Gentisic Acid to lipid ratio (nGA/nlip from 10-5 to 1) on membrane fluidity and thermotropic properties. Multilamellar vesicles of phosphatidylcholines (with size range between 1350 and 1900 nm) effectively encapsulated GA (54%) when nGA/nlip was higher than 0.01. Suppression of lipid peroxidation was directly related to concentration of GA. The resistance to diffusion of Gentisic Acid from liposomes increased for ˜50% in samples incorporating 50 mol % β-sitosterol compared to sterol-free liposomes. Finally, simulated in vitro gastrointestinal conditions showed that the release was mainly affected by low pH of simulated gastric fluid and the presence of cholates in simulated intestinal fluid, rather than by enzymes activity.
Brett K Kaiser - One of the best experts on this subject based on the ideXlab platform.
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Siderocalin/Lcn2/NGAL/24p3 Does Not Drive Apoptosis Through Gentisic Acid Mediated Iron Withdrawal in
2016Co-Authors: Hematopoietic Cell Lines, Matthew C. Clifton, Colin Correnti, Vera Richardson, Allyson K Sia, Mario Ruiz, Margaret A Holmes, Ashok D. B, Suryo Rahmanto, Brett K KaiserAbstract:Siderocalin (also lipocalin 2, NGAL or 24p3) binds iron as complexes with specific siderophores, which are low molecular weight, ferric ion-specific chelators. In innate immunity, siderocalin slows the growth of infecting bacteria by sequestering bacterial ferric siderophores. Siderocalin also binds simple catechols, which can serve as siderophores in the damaged urinary tract. Siderocalin has also been proposed to alter cellular iron trafficking, for instance, driving apoptosis through iron efflux via BOCT. An endogenous siderophore composed of Gentisic Acid (2,5-dihydroxybenzoic Acid) substituents was proposed to mediate cellular efflux. However, binding studies reported herein contradict the proposal that Gentisic Acid forms high-affinity ternary complexes with siderocalin and iron, or that Gentisic Acid can serve as an endogenous siderophore at neutral pH. We also demonstrate that siderocalin does not induce cellular iron efflux or stimulate apoptosis
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siderocalin lcn2 ngal 24p3 does not drive apoptosis through Gentisic Acid mediated iron withdrawal in hematopoietic cell lines
PLOS ONE, 2012Co-Authors: Colin Correnti, Matthew C. Clifton, Vera Richardson, Allyson K Sia, Ashok D Bandaranayake, Mario Ruiz, Yohan Suryo Rahmanto, žaklina Kovacevic, Margaret A Holmes, Brett K KaiserAbstract:Siderocalin (also lipocalin 2, NGAL or 24p3) binds iron as complexes with specific siderophores, which are low molecular weight, ferric ion-specific chelators. In innate immunity, siderocalin slows the growth of infecting bacteria by sequestering bacterial ferric siderophores. Siderocalin also binds simple catechols, which can serve as siderophores in the damaged urinary tract. Siderocalin has also been proposed to alter cellular iron trafficking, for instance, driving apoptosis through iron efflux via BOCT. An endogenous siderophore composed of Gentisic Acid (2,5-dihydroxybenzoic Acid) substituents was proposed to mediate cellular efflux. However, binding studies reported herein contradict the proposal that Gentisic Acid forms high-affinity ternary complexes with siderocalin and iron, or that Gentisic Acid can serve as an endogenous siderophore at neutral pH. We also demonstrate that siderocalin does not induce cellular iron efflux or stimulate apoptosis, questioning the role siderocalin plays in modulating iron metabolism.
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Siderocalin/Lcn2/NGAL/24p3 Does Not Drive Apoptosis Through Gentisic Acid Mediated Iron Withdrawal in Hematopoietic Cell Lines
2012Co-Authors: Colin Correnti, Matthew C. Clifton, Vera Richardson, Allyson K Sia, Ashok D Bandaranayake, Mario Ruiz, Yohan Suryo Rahmanto, Margaret A Holmes, Žaklina Kovačević, Brett K KaiserAbstract:Siderocalin (also lipocalin 2, NGAL or 24p3) binds iron as complexes with specific siderophores, which are low molecular weight, ferric ion-specific chelators. In innate immunity, siderocalin slows the growth of infecting bacteria by sequestering bacterial ferric siderophores. Siderocalin also binds simple catechols, which can serve as siderophores in the damaged urinary tract. Siderocalin has also been proposed to alter cellular iron trafficking, for instance, driving apoptosis through iron efflux via BOCT. An endogenous siderophore composed of Gentisic Acid (2,5-dihydroxybenzoic Acid) substituents was proposed to mediate cellular efflux. However, binding studies reported herein contradict the proposal that Gentisic Acid forms high-affinity ternary complexes with siderocalin and iron, or that Gentisic Acid can serve as an endogenous siderophore at neutral pH. We also demonstrate that siderocalin does not induce cellular iron efflux or stimulate apoptosis, questioning the role siderocalin plays in modulating iron metabolism.
Paul Fernyhough - One of the best experts on this subject based on the ideXlab platform.
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Gentisic Acid sodium salt a phenolic compound is superior to norepinephrine in reversing cardiovascular collapse hepatic mitochondrial dysfunction and lactic Acidemia in pseudomonas aeruginosa septic shock in dogs
Intensive Care Medicine Experimental, 2016Co-Authors: Steven N. Mink, Subir Roy K Chowdhury, Jose Gotes, Zhaoqin Cheng, Krika Kasian, Paul FernyhoughAbstract:Background The development of lactic Acidemia (LA) in septic shock (SS) is associated with an ominous prognosis. We previously showed that the mechanism of LA in SS may relate to impaired hepatic uptake of lactate, but the mechanism was not clear. Uptake of lactate by the liver occurs by a membrane-associated, pH-dependent, antiport system known as the monocarboxylate transporter. In the hepatocyte, lactate can then be metabolized by oxidative phosphorylation or converted to glucose in the cytosol. In the present study, we examined (1) whether hepatic mitochondrial dysfunction accounted for decreased uptake of lactate in a canine model of Pseudomonas aeruginosa SS, (2) whether norepinephrine (NE) treatment by increasing mean arterial pressure (MAP) could improve mitochondrial dysfunction and LA in this model, and (3) whether Gentisic Acid sodium salt (GSS), a novel phenolic compound, was superior to NE in these effects.
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Gentisic Acid sodium salt a phenolic compound is superior to norepinephrine in reversing cardiovascular collapse hepatic mitochondrial dysfunction and lactic Acidemia in pseudomonas aeruginosa septic shock in dogs
Intensive Care Medicine Experimental, 2016Co-Authors: Steven N. Mink, Subir Roy K Chowdhury, Jose Gotes, Zhaoqin Cheng, Krika Kasian, Paul FernyhoughAbstract:The development of lactic Acidemia (LA) in septic shock (SS) is associated with an ominous prognosis. We previously showed that the mechanism of LA in SS may relate to impaired hepatic uptake of lactate, but the mechanism was not clear. Uptake of lactate by the liver occurs by a membrane-associated, pH-dependent, antiport system known as the monocarboxylate transporter. In the hepatocyte, lactate can then be metabolized by oxidative phosphorylation or converted to glucose in the cytosol. In the present study, we examined (1) whether hepatic mitochondrial dysfunction accounted for decreased uptake of lactate in a canine model of Pseudomonas aeruginosa SS, (2) whether norepinephrine (NE) treatment by increasing mean arterial pressure (MAP) could improve mitochondrial dysfunction and LA in this model, and (3) whether Gentisic Acid sodium salt (GSS), a novel phenolic compound, was superior to NE in these effects. In anesthetized/ventilated dogs, we infused the bacteria over ~10 h and measured hemodynamics in various treatment groups (see below). We then euthanized the animal and isolated the hepatic mitochondria. We measured hepatic mitochondrial oxygen consumption rates using the novel Seahorse XF24 analyzer under conditions that included: basal respiration, after the addition of adenosine- diphosphate to produce coupled respiration, and after the addition of a protonophore to produce maximal respiration. We found that in the septic control group, mean arterial pressure decreased over the course of the study, and that mitochondrial dysfunction developed in which there was a reduction in maximal respiration. Whereas both NE and GSS treatments reversed the reduction in mean arterial pressure and increased maximal respiration to similar extents in respective groups, only in the GSS group was there a reduction in LA. Hepatic mitochondrial dysfunction occurs in SS, but does not appear to be required for the development of LA in SS, since NE improved mitochondrial dysfunction without reversing LA. GSS, a phenolic compound restored mean arterial pressure, mitochondrial dysfunction, and LA in SS. This reduction in LA may be independent of its effect on improving hepatic mitochondrial function.
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Additional file 1: of Gentisic Acid sodium salt, a phenolic compound, is superior to norepinephrine in reversing cardiovascular collapse, hepatic mitochondrial dysfunction and lactic Acidemia in Pseudomonas aeruginosa septic shock in dogs
2016Co-Authors: Steven Mink, Jose Gotes, Zhaoqin Cheng, Krika Kasian, Subir Roy Chowdhury, Paul FernyhoughAbstract:Figure S1. In this figure, troponin, our index of myocardial injury, increased in the NE septic group, while it did not change in the other groups. GSS is Gentisic Acid sodium salt. Statistical analyses included two-way repeated measures analysis of variance and Student Newman Keuls (SNK) multiple comparison multiple comparison test. (DOC 170Â kb