RESUMEN
The present work aimed to estimate the possible anti-fatigue effect and potential mechanism of Isochrysis galbana (IG) in mice. The anti-fatigue activity of IG (100, 200, and 400 mg/kg) was elucidated by a weight-loaded forced swimming test, and the potential mechanism was explored by determination of fatigue-related biochemical parameters. The results showed that pretreatment with IG significantly extended the exhaustive swimming time and increased the levels of liver glycogen, muscle glycogen and blood glucose in a dose-dependent manner. Besides, the increased levels of alanine aminotransferase, aspartate aminotransferase, blood lactic acid, lactic dehydrogenase, creatine kinase, and blood urea nitrogen by exhausted swimming, were dramatically attenuated by pretreatment with IG. Furthermore, supplementation with IG significantly enhanced the glutathione peroxidase and superoxide dismutase levels, while attenuated the level of malonaldehyde. Taken together, IG possessed appreciable efficacy to alleviate fatigue, and the mechanism might be associated with favorably modulating the process of energy consumption, metabolism, and attenuating oxidative stress injury.
RESUMEN
Single-cell sequencing technologies can be used to detect the genome, transcriptome and other multi-omics of single cells. They can show the differences and evolutionary relationships of various cells. This review introduces the latest advances in single-cell sequencing technologies and their applications in oncology, microbiology, neurology, reproduction, immunology, digestive and urinary systems, highlighting the important role that single-cell sequencing techniques play in these areas.
RESUMEN
CHD5 is an essential factor for neuronal differentiation and neurodegenerative diseases. Here, the targeted next generation sequencing and TaqMan genotyping technologies were carried out for CHD5 gene in a two-staged case-control study in Chinese population. The genetic statistics and gene-environment interactions were analyzed to find certain risk factors of Alzheimer's disease. We found intronic rs11121295 was associated with the risk of Alzheimer's disease at both stages including combined cohorts. This risk effect presented consistently significant associations with the alcoholic subgroups at both all stages in the stratified analysis. The gene-environment interactions further supported the above findings. Our study highlighted the potential role of CHD5 variants in conferring susceptibility to sporadic Alzheimer's disease, especially modified its risk by alcoholic intake.
RESUMEN
Previous studies showed that the low expressions of chromodomain-helicase-DNA-binding protein 5 (CHD5) were intensively associated with deteriorative biologic and clinical characteristics as well as outcomes in many tumors. The aim of this study is to determine whether CHD5 single nucleotide polymorphisms (SNPs) contribute to the prognosis of hepatocellular carcima (HCC). The SNPs were selected according to their linkage disequilibrium (LD) in the targeted next-generation sequencing (NGS) and then genotyped with TaqMan probers. We revealed a rare haplotype AG in CHD5 (SNPs: rs12564469-rs9434711) was markedly associated with HCC prognosis. The univariate and multivariate regression analyses revealed the patients with worse overall survival time were those with tumor metastasis and haplotype AG, as well as cirrhosis, poor differentiation and IV-TNM stage. Based on the available public databases, we discovered the significant association between haplotype AG and CHD5 mRNA expressions only existed in Chinese. These data proposed that the potentially genetic haplotype might functionally contribute to HCC prognosis and CHD5 mRNA expressions.
RESUMEN
In the present study, we investigated the neuroprotective effects of GPP1, a purified polysaccharide from Gynostemma pentaphyllum, on Aß (25-35)-induced neuronal toxicity and explore its potential mechanisms in PC12 cells. The results showed pretreatment with GPP1 prior to Aß (25-35) exposure significantly protected PC12 cells from Aß (25-35)-induced cell death, lactate dehydrogenase (LDH) release, DNA damage, intracellular free calcium concentration ([Ca(2+)]i) influx, mitochondrial dysfunction and mitochondrial cytochrome c (Cyt-C) release. In addition, pretreatment with GPP1 also protected PC12 cells against Aß (25-35)-induced the accumulation of reactive oxygen species (ROS) and lipid peroxidation product MDA, the reduction in glutathione (GSH) level and superoxide dismutase (SOD) activity, the increased Bax/Bcl-2 protein expression ratio and caspase-3 activation. Our findings suggest that GPP1 exerts a neuroprotective effect against Aß (25-35)-induced neurotoxicity in PC12 cells, at least in part, via inhibiting oxidative stress and suppressing the mitochondrial apoptotic pathway.
