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91.
Synthesis of β‐Ketoamide Curcumin Analogs for Anti‐Diabetic and AGEs Inhibitory Activities
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Govindharasu Banuppriya Rajendran Sribalan Sulthan Alavudeen Rizwan Fathima Vediappen Padmini 《化学与生物多样性》2018,15(8)
Two different series of novel β‐ketoamide curcumin analogs enriched in biological activities have been synthesized. The synthesized compounds were screened for their in vitro anti‐diabetic and AGEs inhibitory activities and exhibited potent to good anti‐diabetic and AGEs inhibitory activities. The molecular docking study was also performed with the α‐amylase enzyme. 相似文献
92.
Mousa Bohlooli Mansour Ghaffari-Moghaddam Mostafa Khajeh Zohre Aghashiri Nader Sheibani Ali Akbar Moosavi-Movahedi 《Journal of biomolecular structure & dynamics》2016,34(12):2658-2666
Acetoacetate (AA) is an important ketone body, which produces reactive oxygen species (ROS). Advanced glycation end products (AGEs) are defined as final products of glycation process whose production is influenced by the levels of ROS. The accumulation of AGEs in the body contributes to pathogenesis of many diseases including complications of diabetes, and Alzheimer’s and Parkinson’s disease. Here, we evaluated the impact of AA on production of AGEs upon incubation of human serum albumin (HSA) with glucose. The effect of AA on the AGEs formation of HSA was studied under physiological conditions after incubation with glucose for 35 days. The physical techniques including circular dichroism (CD) and fluorescence spectroscopy were used to assess the impact of AA on formation and structural changes of glycated HSA (GHSA). Our results indicated that the secondary and tertiary structural changes of GHSA were increased in the presence of AA. The fluorescence intensity measurements of AGEs also showed an increase in AGEs formation. Acetoacetate has an activator effect in formation of AGEs through ROS production. The presence of AA may result in enhanced glycation in the presence of glucose and severity of complications associated with accumulation of AGEs. 相似文献
93.
Guanosine 5'-triphosphate (GTP) plays a significant role in the bioenergetics, metabolism, and signaling of cells; consequently, any modifications to the structure of the molecule can have profound effects on a cell's survival and function. Previous studies in our laboratory demonstrated that like proteins, purines, and pyrimidines can nonenzymatically react with sugars to generate advanced glycation endproducts (AGEs) and that these AGEs can form in vitro under physiological conditions. The objective of this investigation was twofold. First, it was to evaluate the susceptibility of ATP, GTP, CTP, and TTP to nonenzymatic modification by D-glucose and DL-glyceraldehyde, and second to assess the effect of various factors such as temperature, pH and incubation time, and sugar concentration on the rate and extent of nucleotide triphosphate AGE formation. Of the four nucleotide triphosphates that were studied, only GTP was significantly reactive forming a heterogeneous group of compounds with DL-glyceraldehyde. D-Glucose exhibited no significant reactivity with any of the nucleotide triphosphates, a finding that was supported by UV and fluorescence spectroscopy. Capillary electrophoresis, high-performance liquid chromatography and mass spectrometry allowed for a thorough analysis of the glycated GTP products and demonstrated that the modification of GTP by dl-glyceraldehyde occurred via the classical Amadori pathway. 相似文献
94.
Marinos Kosmopoulos Dimitrios Drekolias Phaedon D. Zavras Christina Piperi Athanasios G. Papavassiliou 《生物化学与生物物理学报:疾病的分子基础》2019,1865(3):611-619
Coronary artery disease remains the leading cause of mortality in adult diabetic population with however, a high predominance also in non-diabetic subjects. In search of common molecular mechanisms and metabolic by-products with potential pathogenic role, increased advanced glycation end products (AGEs) present a critical biomarker for CAD development in both cases. Interaction of AGEs with their transmembrane cell receptor, RAGE in endothelial and smooth muscle cells as well as in platelets, activates intracellular signaling that leads to endothelial injury, modulation of vascular smooth muscle cell function and altered platelet activity. Furthermore, tissue accumulation of AGEs affects current treatment approaches being involved in stent restenosis. The present review provides an update of AGE-induced molecular mechanisms involved in CAD pathophysiology while it discusses emerging therapeutic interventions targeting AGE reduction and AGE-RAGE signaling with beneficial clinical outcome. 相似文献
95.
摘要 目的:探讨血清胱抑素C(Cys-C)、总胆红素(TBiL)、肾上腺髓质中段肽(MR-proADM)、晚期糖基化终末产物(AGEs)与老年慢性心力衰竭(CHF)患者心功能和心脏再同步化治疗(CRT)应答的关系。方法:选择2020年3月至2022年1月我院收治的151例接受CRT治疗的老年CHF患者为研究对象,随访6个月,统计治疗应答情况。CRT治疗前检测血清Cys-C、TBiL、MR-proADM、AGEs水平,超声心动图检测心功能,分析血清Cys-C、TBiL、MR-proADM、AGEs与心功能的相关性以及与老年CHF患者CRT治疗应答的关系。结果:151例患者失访1例,余150例患者中无应答48例(无应答组),应答102例(应答组)。无应答组血清Cys-C、TBiL、MR-proADM、AGEs水平均高于应答组(P<0.05),且与左心室射血分数(LVEF)呈负相关(P<0.05),与左室舒张末期内径(LVEDD)和左室收缩末期内径(LVESD)呈正相关(P<0.05)。多因素Logistic回归分析结果显示缺血性心肌病、血清Cys-C、TBiL、MR-proADM、AGEs是老年CHF患者CRT治疗无应答的危险因素(P<0.05),LVEF是保护因素(P<0.05)。结论:CRT治疗无应答老年CHF患者血清Cys-C、TBiL、MR-proADM、AGEs水平升高,且与心功能下降有关。血清Cys-C、TBiL、MR-proADM、AGEs是CRT治疗无应答的危险因素,可为CRT治疗效果评估提供一定的参考。 相似文献
96.
吡哆胺-一种天然的AGEs/ALEs抑制剂 总被引:2,自引:0,他引:2
衰老及老年相关疾病,如:糖尿病、动脉粥状硬化、各种神经退行性疾病等,与组织蛋白氧化修饰密切相关.在造成蛋白质氧化修饰的反应中,非酶糖基化和脂质过氧化是最重要的两类,它们最终形成非酶糖基化终产物(AGEs)和脂过氧化终产物(ALEs).基于羰基毒害衰老理论,具有强烈反应活性的羰基类化合物是非酶糖基化和脂质过氧化的共同中间产物,它们是造成蛋白修饰的直接原因之一.吡哆胺是维生素B6的一种天然成分;由于它能直接清除羰基类化合物,从而抑制AGEs/ALEs的生成;又因为吡哆胺对人体副作用很小.因此吡哆胺有望成为一种新型的防治多种老年相关疾病的药物. 相似文献
97.
Nana Kato Satoko Kawabe Natsuki Ganeko Morio Yoshimura Yoshiaki Amakura 《Bioscience, biotechnology, and biochemistry》2017,81(7):1285-1288
We investigated the inhibitory effects of several plant extracts on advanced glycation end-products (AGEs) formation. Among tested samples, the flower extract of Magnolia coco showed significant inhibition of AGE formation. We isolated and characterized procyanidin oligomer and four other compounds from the flowers, and evaluated their inhibitory effects on AGE formation and the AGE-derived crosslink-cleaving activity of the isolated compounds. 相似文献
98.
Mathys KC Ponnampalam SN Padival S Nagaraj RH 《Biochemical and biophysical research communications》2002,297(4):863-869
Semicarbazide-sensitive amine oxidase (SSAO) catalyzes formation of methylglyoxal (MG) from aminoacetone; MG then reacts with proteins to form advanced glycation end products or AGEs. Because of its potential to generate MG, SSAO may contribute to AGE-associated vascular complications of aging and diabetes. We developed a method to measure SSAO activity in bovine aortic smooth muscle cells (BASMC) based on the oxidation of 2',7'-dichlorofluorescin by hydrogen peroxide and horseradish peroxidase. The SSAO activity was completely inhibited by 10 mM semicarbazide. Argpyrimidine is a readily detectable fluorescent product of the reaction between MG and arginine. Cell lysates incubated with aminoacetone formed argpyrimidine in a reaction that was inhibited by 20 mM semicarbazide. Immunostaining of tissue sections showed that aminoacetone-treated rats (normal as well as diabetic) formed more argpyrimidine in aortic smooth muscle than untreated controls. We believe that SSAO can enhance AGE synthesis in the macrovasculature of diabetic individuals by production of MG. 相似文献
99.
Nagaraj RH Sarkar P Mally A Biemel KM Lederer MO Padayatti PS 《Archives of biochemistry and biophysics》2002,402(1):110-119
Advanced glycation end products (AGEs) from the Maillard reaction contribute to protein aging and the pathogenesis of age- and diabetes-associated complications. The alpha-dicarbonyl compound methylglyoxal (MG) is an important intermediate in AGE synthesis. Recent studies suggest that pyridoxamine inhibits formation of advanced glycation and lipoxidation products. We wanted to determine if pyridoxamine could inhibit MG-mediated Maillard reactions and thereby prevent AGE formation. When lens proteins were incubated with MG at 37 degrees C, pH 7.4, we found that pyridoxamine inhibits formation of methylglyoxal-derived AGEs concentration dependently. Pyridoxamine reduces MG levels in red blood cells and plasma and blocks formation of methylglyoxal-lysine dimer in plasma proteins from diabetic rats and it prevents pentosidine (an AGE derived from sugars) from forming in plasma proteins. Pyridoxamine also decreases formation of protein carbonyls and thiobarbituric-acid-reactive substances in plasma proteins from diabetic rats. Pyridoxamine treatment did not restore erythrocyte glutathione (which was reduced by almost half) in diabetic animals, but it enhanced erythrocyte glyoxalase I activity. We isolated a major product of the reaction between MG and pyridoxamine and identified it as methylglyoxal-pyridoxamine dimer. Our studies show that pyridoxamine reduces oxidative stress and AGE formation. We suspect that a direct interaction of pyridoxamine with MG partly accounts for AGE inhibition. 相似文献
100.
Effects of thermal denaturation on protein glycation 总被引:4,自引:0,他引:4
Protein denaturation occurs at sites of inflammation. We hypothesized that denatured protein may provide a more susceptible target for glycation, which is a known mediator of inflammation. We examined the effects of thermal denaturation on the susceptibility of protein glycation using glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and aspartate aminotransferase (AAT) as our target proteins. GAPDH and AAT are ubiquitous proteins that exhibited very different thermal stabilities. Glycating agents, methylglyoxal (MG) and glyceraldehyde (Glyc), caused an increase in the formation of advanced glycation endproducts (AGEs) in native and denatured GAPDH and AAT. The effects of the glycating agents were more pronounced with the denatured proteins. In addition to nitroblue tetrazolium (NBT)- reactivity, our measured endpoints were absorbance (lambda = 365 nm) and fluorescence (lambda(ex) = 370 nm; lambda(em) = 470 nm) properties that are typically associated with protein glycation. We also looked at carnosine's ability to prevent glycation of native and denatured protein. Carnosine, an endogenous histidine dipeptide, exhibits anti-inflammatory activity presumably due to its anti-oxidant and anti-glycation properties. Carnosine prevented Glyc-induced AGE formation in both native and denatured AAT suggesting that carnosine's anti-inflammatory activity may be due in part to carnosine's ability to prevent glycation of denatured protein. 相似文献