NMR-Based Metabolomics Approach to Investigate the Effects of Fruits of Acanthopanax sessiliflorus in a High-Fat Diet Induced Mouse Model

The prevalence of obesity is rapidly increasing and is recognized as a serious health problem. To investigate metabolic changes in an obese model after administration of Acanthopanax sessiliflorus, mice were divided into four groups: normal diet, high-fat diet (HFD), HFD with treatment fenofibrate, and A. sessiliflorus fruit extract. The liver tissue of mice was analyzed using nuclear magnetic resonance (NMR) spectrometry-based metabolomics. In multivariate statistical analyses, the HFD group was discriminated from the normal diet group, and the group fed A. sessiliflorus fruit was discriminated from the HFD group. In biomarker analysis between the HFD group and the group fed A. sessiliflorus fruit, alanine, inosine, formate, pyroglutamate, taurine, and tyrosine, with AUC values of 0.7 or more, were found. The levels of these metabolites were distinguished from the HFD mouse model. Changes in these metabolites were confirmed to act on metabolic pathways related to antioxidant activity

Antioxidant Efficacy of Hwangryunhaedok-tang through Nrf2 and AMPK Signaling Pathway against Neurological Disorders In Vivo and In Vitro

Alzheimer’s disease (AD) is a representative cause of dementia and is caused by neuronal loss, leading to the accumulation of aberrant neuritic plaques and the formation of neurofibrillary tangles. Oxidative stress is involved in the impaired clearance of amyloid beta (Aβ), and Aβ-induced oxidative stress causes AD by inducing the formation of neurofibrillary tangles. Hwangryunhaedok-tang (HHT, Kracie K-09®), a traditional herbal medicine prescription, has shown therapeutic effects on various diseases. However, the studies of HHT as a potential treatment for AD are insufficient. Therefore, our study identified the neurological effects and mechanisms of HHT and its key bioactive compounds against Alzheimer’s disease in vivo and in vitro. In a 5xFAD mouse model, our study confirmed that HHT attenuated cognitive impairments in the Morris water maze (MWM) test and passive avoidance (PA) test. In addition, the prevention of neuron impairment, reduction in the protein levels of Aβ, and inhibition of cell apoptosis were confirmed with brain tissue staining. In HT-22 cells, HHT attenuates tBHP-induced cytotoxicity, ROS generation, and mitochondrial dysfunction. It was verified that HHT exerts a neuroprotective effect by activating signaling pathways interacting with Nrf2, such as MAPK/ERK, PI3K/Akt, and LKB1/AMPK. Among the components, baicalein, a bioavailable compound of HHT, exhibited neuroprotective properties and activated the Akt, AMPK, and Nrf2/HO-1 pathways. Our findings indicate a mechanism for HHT and its major bioavailable compounds to treat and prevent AD and suggest its potential

Realizing the potential of hydrophobic crystalline carbon as a support for oxygen evolution electrocatalysts

Anion exchange membrane water electrolysis (AEMWE) is a sustainable solution for achieving net-zero carbon emissions and meeting growing energy demands through green H-2 production. However, its commercialization has not been realized thus far owing to inefficient catalyst use and unsatisfactory performance, which are correlated to the inadequacy of current electrode structures. In this study, we developed an efficient electrode structure based on a corrosion-resistant hydrophobic crystalline carbon support, which was incorporated as a support for Fe-Ni-Co layered double hydroxide electrocatalysts. We observed an AEMWE performance greater than that reported in previous studies in terms of activity [mass-specific power (24.1 kW g(metal)(-1))] and durability (-0.06 mV h(-1) for 520 h at 1.0 A cm(-2)). This could be attributed to the improved mass transport because of rapid water diffusion around the hydrophobic carbon and strong metal-carbon interactions. We believe that this study will promote the development of more carbon-supported oxygen evolution reaction electrocatalysts.11Nsciescopu

Clinical characteristics of the study subjects stratified by time-averaged serum sodium level.

<p>Values for categorical variables are given as number (percentage); values for continuous variables are given as mean ± standard deviation or median [interquartile range].</p><p>*Laboratory and dialysis-specific parameters are given as time-averaged values. GFR, glomerular filtration rate; nPCR, normalized protein catabolic rate; ACE, angiotensin converting enzyme; ARB, angiotensin receptor blocker.</p><p>Clinical characteristics of the study subjects stratified by time-averaged serum sodium level.</p

Multivariable Cox regression analyses for all-cause, cardiovascular, and infection-related mortality.

<p>TA-Na, time-averaged serum sodium; HR, hazard ratio; CI, confidence interval. Model 1 adjusted for epidemiologic parameters including age, sex, body mass index, and Charlson Comorbidity Index score. Model 2 adjusted for all model 1 parameters plus medication including dose of furosemide, use of icodextrin, and use of high glucose dialysate. Model 3 adjusted for all model 2 parameters plus dialysis dose including peritoneal dialysis ultrafiltration (PDUF) and total Kt/V urea. Model 4 adjusted for all model 3 parameters plus malnutrition-inflammatory parameters including serum potassium, serum bicarbonate, serum albumin, serum ferritin, C-reactive protein (CRP), residual glomerular filtration rate (GFR), normalized protein catabolic rate (nPCR), and percentage of lean body mass (%LBM). Laboratory (serum sodium, potassium, bicarbonate, albumin, ferritin, and CRP) and dialysis-specific (PDUF, Kt/V urea, residual GFR, nPCR, %LBM) parameters are given as time-averaged values.</p><p>Multivariable Cox regression analyses for all-cause, cardiovascular, and infection-related mortality.</p

Cross-sectional correlation analyses between baseline serum sodium level and patient characteristics.

<p>*Data for ferritin, CRP, and residual GFR were log-transformed.</p><p>BMI, body mass index; CCI, Charlson Comorbidity Index score; Na, sodium; K, serum potassium; tCO2, serum bicarbonate; CRP, C-reactive protein; GFR, glomerular filtration rate; PD UF, peritoneal dialysis ultrafiltration; nPCR, normalized protein, LBM, percentage of lean body mass.</p><p>Cross-sectional correlation analyses between baseline serum sodium level and patient characteristics.</p

Flow chart of participants in the cohort.

<p>PD, peritoneal dialysis; HD, hemodialysis; KT, kidney transplant.</p

The Cumulative incidence of all-cause (A), cardiovascular (B), and infection-related (C) mortality based on the level of time-averaged serum sodium (TA-Na).

<p>The Cumulative incidence of all-cause (A), cardiovascular (B), and infection-related (C) mortality based on the level of time-averaged serum sodium (TA-Na).</p