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Background The growing interest in identifying the mode of action of traditional medicines has strengthened its research. Syzygium jambolanum (Syzyg) is commonly prescribed in homeopathy and is a rich source of phytochemicals. Objective The present study aims to shed light on the anti-glycation molecular mechanism of Syzyg mother tincture (MT), 30c, and 200c on glycated human serum albumin (HSA) by multi-spectroscopic and microscopic approaches. Methods The phytochemicals and antioxidant potential of the Syzyg formulations were estimated by the high-performance liquid chromatography and spectroscopic technique, respectively. Glycation was initiated by incubating HSA with methylglyoxal, three Syzyg formulations, and the known inhibitor aminoguanidine in separate tubes at 37°C for 48 hours. The formation of glycation adducts was assessed by spectrofluorometer and affinity chromatography. The structural modifications were analyzed through circular dichroism, Fourier transform infrared spectroscopy, turbidity, 8-anilinonapthalene-1-sulfonic acid fluorescence, and nuclear magnetic resonance. Further, the formation of the aggregates was examined by thioflavin T, native-polyacrylamide gel electrophoresis, and transmission electron microscopy. Additionally, the functional modifications of glycated HSA were determined by esterase-like activity and antioxidant capacity. The binding analysis of Syzyg formulations with glycated HSA was evaluated by surface plasmon resonance (SPR). Results Syzyg formulations MT, 30c, and 200c contained gallic acid and ellagic acid as major phytochemicals, with concentrations of 16.02, 0.86, and 0.52 µg/mL, and 227.35, 1.35, and 0.84 µg/mL, respectively. Additionally, all three formulations had remarkable radical scavenging ability and could significantly inhibit glycation compared with aminoguanidine. Further, Syzyg formulations inhibited albumin's structural and functional modifications. SPR data showed that Syzyg formulations bind to glycated HSA with an equilibrium dissociation constant of 1.10 nM. Conclusion Syzyg formulations inhibited the glycation process while maintaining the structural and functional integrity of HSA. [ABSTRACT FROM AUTHOR]

One of the most popular drinks in the world, tea is a member of the family Theaceae, obtained from the plant Camellia Sinensis, found explicitly in humid and warm regions, attracts interest for its flavour and scent as well as its advantageous health properties. It is divided into three main categories: unfermented green tea and white tea, partially fermented oolong tea, and black tea that has undergone fermentation. Green tea is currently the psychostimulant most often used worldwide, as it has been shown to enhance cognitive thinking, improve neuromuscular coordination, and reduce tension and anxiety. However, it also contains caffeine members of methylxanthines which, in high amounts, more than its moderate dose, i.e., 400mg/day, can cause significant toxicity and even lethality showing symptoms such as involuntary contraction of the muscles, failure of the respiration, and heart, coma, migraine, or even death of the person in adverse cases. This study's objective is to determine the qualitative content of caffeine released in green tea after boiling over time. Liquid chromatography is used for the detection of caffeine. To establish a more exact relation between the amounts of caffeine taken and its physiological effects, it is crucial to create more accurate, easy, and quick procedures for the detection of caffeine. Caffeine was successfully eluted using this technique in three minutes, with a few additional peaks. The standard calibration curve showed exemplary linearity, and the correlation coefficient was above 0.9983. [ABSTRACT FROM AUTHOR]

Silver nanoparticles have many medical and commercial applications, but their effects on human health are poorly understood. They are used extensively in products of daily use, but little is known about their potential neurotoxic effects. A xenobiotic metal, silver, has no known physiological significance in the human body as a trace metal. Biokinetics of silver nanoparticles indicates its elimination from the body via urine and feces route. However, a substantial amount of evidence from both in vitro and in vivo experimental research unequivocally establish the fact of easier penetration of smaller nanoparticles across the blood–brain barrier to enter in brain and thereby interaction with cellular components to induce neurotoxic effects. Toxicological effects of silver nanoparticles rely on the degree of exposure, particle size, surface coating, and agglomeration state as well as the type of cell or organism used to evaluate its toxicity. This review covers pertinent facts and the present state of knowledge about the neurotoxicity of silver nanoparticles reviewing the impacts on oxidative stress, neuroinflammation, mitochondrial function, neurodegeneration, apoptosis, and necrosis. The effect of silver nanoparticles on the central nervous system is a topic of growing interest and concern that requires immediate consideration. Concerns about environmental safety and human health have arisen due to the growing use of AgNPs for various applications. According to our findings, even though physicochemical characteristics determine neurotoxicity, AgNPs elicit at least a minimal level of toxicity independent of their attributes. The finding also suggests AgNP‐induced ROS as the root cause of toxicity within the CNS, resulting in oxidative stress, inflammation, apoptosis, necrosis, mitochondrial dysfunction, and disruption of intracellular calcium homeostasis, eventually leading to cell death. [ABSTRACT FROM AUTHOR]

ABSTRACT The sulfonylurea urea drug glyburide (glibenclamide) is widely used for the treatment of diabetes milletus and gestational diabetes. In previous studies monohydroxylated metabolites were identified and characterized for glyburide in different species, but the metabolite owing to the loss of cyclohexyl ring was identified only in mouse. Glyburide upon incubation with hepatic microsomes resulted in 10 metabolites for human. The current study identifies new metabolites of glyburide along with the hydroxylated metabolites that were reported earlier. The newly identified drug metabolites are dihydroxylated metabolites, a metabolite owing to the loss of cyclohexyl ring and one owing to hydroxylation with dehydrogenation. Among the 10 identified metabolites, there were six monohydroxylated metabolites, one dihydroxylated metabolite, two metabolites owing to hydroxylation and dehydrogenation, and one metabolite owing to the loss of cyclohexyl ring. New metabolites of glyburide were identified and characterized using liquid chromatography-diode array detector-quadruple-ion trap-mass spectrometry/mass spectrometry (LC-DAD-Q-TRAP-MS/MS). An enhanced mass scan-enhanced product ion scan with information-dependent acquisition mode in a Q-TRAP-MS/MS system was used to characterize the metabolites. Liquid chromatography with diode array detection was used as a complimentary technique to confirm and identify the metabolites. Metabolites formed in higher amounts were detected in both diode array detection and mass spectrometry detection. Copyright © 2012 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]