Age-related macular degeneration (AMD) is the leading cause of vision loss among the elderly, which is primarily attributed to oxidative stress-induced damage to the retinal pigment epithelium (RPE). Human amniotic mesenchymal stem cells (hAMSC) were considered to be one of the most promising stem cells for clinical application due to their low immunogenicity, tissue repair ability, pluripotent potential and potent paracrine effects. The conditional medium (hAMSC-CM) and exosomes (hAMSC-exo) derived from hAMSC, as mediators of intercellular communication, play an important role in the treatment of retinal diseases, but their effect and mechanism on oxidative stress-induced retinal degeneration are not explored. Here, we reported that hAMSC-CM alleviated H2O2-induced ARPE-19 cell death through inhibiting mitochondrial-mediated apoptosis pathway in vitro. The overproduction of reactive oxygen species (ROS), alteration in mitochondrial morphology, loss of mitochondrial membrane potential and elevation of Bax/Bcl2 ratio in ARPE-19 cells under oxidative stress were efficiently reversed by hAMSC-CM. Moreover, it was found that hAMSC-CM protected cells against oxidative injury via PI3K/Akt/FoxO3 signaling. Intriguingly, exosome inhibitor GW4869 alleviated the inhibitory effect of hAMSC-CM on H2O2-induced decrease in cell viability of ARPE-19 cells. We further demonstrated that hAMSC-exo exerted the similar protective effect on ARPE-19 cells against oxidative damage as hAMSC-CM. Additionally, both hAMSC-CM and hAMSC-exo ameliorated sodium iodate-induced deterioration of RPE and retinal damage in vivo. These results first indicate that hAMSC-CM and hAMSC-exo protect RPE cells from oxidative damage by regulating PI3K/Akt/FoxO3 pathway, suggesting hAMSC-CM and hAMSC-exo will be a promising cell-free therapy for the treatment of AMD in the future.
BACKGROUND: L-lysine (lysine) is an essential amino acid that plays a vital role in human nutrition. It serves as a key component in protein synthesis and fulfills critical roles in various physiological activities. For decades, lysine supplements have been extensively used to promote the growth and development of children, particularly in developing countries where cereal-based diets are everyday staples. AIM OF THE REVIEW: This review aims to provide an overview of the overall effectiveness of lysine supplements concerning the growth of children and adolescents. Additionally, it addresses the potential precautions that should be considered when using lysine supplements in this context. KEY SCIENTIFIC CONCEPTS OF REVIEW: Receiving lysine oral supplements and lysine-fortified cereal diets were observed to enhance nitrogen retention and improve anthropometric measurements such as height, weight, Z-scores, body mass index, and skinfold thickness. Furthermore, lysine positively influenced the children's developmental quotient and various serological biochemical parameters, such as hormones, immunological indicators, proteins, bone metabolic indicators, and red blood cell parameters. These supplements are generally considered clinically safe, with no reported toxicity where the related side effects are limited to subjective gastrointestinal tract symptoms. It is essential to be cautious about excessive intake of lysine, as it can lead to an imbalance of amino acids, thereby potentially suppressing its intended benefits. When used with appropriate precautions, lysine can serve as a safe supplement with promising benefits for the growth of children and adolescents. Nevertheless, further contemporary research studies on lysine supplementation would be insightful and valuable in better understanding its optimal use, potential benefits, and safety in promoting growth.
The influence of oat lipids on the structural, thermal, rheological, and in vitro digestibility properties of oat starch under heat processing conditions was investigated. X-ray diffraction, fourier infrared spectroscopy, and differential scanning calorimetry revealed the formation of a V-shaped crystal structure between starch and lipid, resulting in enhanced orderliness and enthalpy. Oat lipids decreased the final viscosity and gel strength of oat starch while weakening the trend towards gel network formation. Additionally, oat lipids exhibited enhanced resistance to starch hydrolase, leading to elevated contents of slowly digestible starch and resistant starch. Consequently, this leads to an augmentation in the rate constants for the rapid digestion fraction (k1) and the slow digestion fraction (k2). When the lipid content reached 7.50 %, a significant increase of 42.20 % was observed in the maximum digestibility of slow digestion fraction (C∞2), while a notable decrease of 44.06 % was noted in the maximum digestibility of rapid digestion fraction (C∞1). The correlation analysis revealed that lipid content, final viscosity, and enthalpy exerted significant influences on in vitro starch digestion. These results demonstrate the substantial impact of lipid content on oat starch structure, subsequently affecting its thermal, rheological, and digestive properties.
BACKGROUND: Prior studies have noted great variability in the plasma levels of risperidone (RIS). Plasma concentrations of RIS and its active moiety are highly variable and depend on absorption, metabolism, and other predictors of metabolic dysregulation; however, these factors are poorly understood and the association between metabolic change and change in psychopathology is uncertain. AIM: To ascertain the characteristics of chronic schizophrenic patients treated with RIS, and to assess their relationship with plasma RIS levels. METHODS: This was a descriptive cross-sectional study of 50 patients with a diagnosis of schizophrenic psychosis treated with RIS in a psychiatric service. The plasma concentrations of RIS and its metabolite 9-hydroxyrisperidone were determined by high performance liquid chromatography. The patients' demographic and clinical characteristics, and psychopathologies were assessed, and the associations between clinical variables and plasma levels of RIS were explored. RESULTS: Male patients received higher doses of RIS than female ones, but plasma concentrations of RIS and risperidone + 9-hydroxyrisperidone (active moiety) were higher in female patients. Age and the mean scores of the general psychopathology subscale of the Positive and Negative Syndrome Scale (PANSS) were significantly positively correlated with plasma concentrations of risperidone + 9-hydroxyrisperidone adjusted for weight and dose in all 50 subjects. In male subjects, we found a statistically significant positive correlation between the concentrations of risperidone + 9-hydroxyrisperidone in plasma/(dose × kg) and age, mean PANSS negative subscale scores, mean PANSS general psychopathology subscale scores, and mean PANSS total scores. CONCLUSION: Long-term use of RIS should be closely monitored in older patients and females to minimize the risk of high concentrations which could induce side effects.
As one of the most urgent social and health problems in the world, neurodegenerative diseases have always been of interest to researchers. However, the pathological mechanisms and therapeutic approaches are not achieved. In addition to the established roles of oxidative stress, inflammation and immune response, changes of gut microbiota are also closely related to the pathogenesis of neurodegenerative diseases. Gut microbiota is the central player of the gut-brain axis, the dynamic bidirectional communication pathway between gut microbiota and central nervous system, and emerging insights have confirmed its indispensability in the development of neurodegenerative diseases. In this review, we discuss the complex relationship between gut microbiota and the central nervous system from the perspective of the gut-brain axis; review the mechanism of microbiota for the modulation different neurodegenerative diseases and discuss how different dietary patterns affect neurodegenerative diseases via gut microbiota; and prospect the employment of gut microbiota in the therapeutic approach to those diseases. © 2024 Society of Chemical Industry.
As important messengers of intercellular communication, exosomes can regulate local and distant cellular communication by transporting specific exosomal contents and can also promote or suppress the development and progression of gastric cancer (GC) by regulating the growth and proliferation of tumor cells, the tumor-related immune response and tumor angiogenesis. Exosomes transport bioactive molecules including DNA, proteins, and RNA (coding and noncoding) from donor cells to recipient cells, causing reprogramming of the target cells. In this review, we will describe how exosomes regulate the cellular immune response, tumor angiogenesis, proliferation and metastasis of GC cells, and the role and mechanism of exosome-based therapy in human cancer. We will also discuss the potential application value of exosomes as biomarkers in the diagnosis and treatment of GC and their relationship with drug resistance.
A wearable Braille-to-speech translation system is of great importance for providing auditory feedback in assisting blind people and people with speech impairment. However, previous reported Braille-to-speech translation systems still need to be improved in terms of comfortability or integration. Here, a Braille-to-speech translation system that uses dual-functional electrostatic transducers which are made of fabric-based materials and can be integrated into textiles is reported. Based on electrostatic induction, the electrostatic transducer can either serve as a tactile sensor or a loudspeaker with the same design. The proposed electrostatic transducers have excellent output performances, mechanical robustness, and working stability. By combining the devices with machine learning algorithms, it is possible to translate the Braille alphabet and 40 commonly used words (extensible) into speech with an accuracy of 99.09% and 97.08%, respectively. This work demonstrates a new approach for further developments of advanced assistive technology toward improving the lives of disabled people.
Lactoferrin (LF), an iron-binding glycoprotein with immunological properties and a high nutritional value, has emerged as a prominent research focus in the field of food nutrition. Lactoferrin is widely distributed in raw milk and milk that has undergone low-temperature heat treatment during pasteurization, making its rapid and accurate detection crucial for ensuring the quality control of dairy products. An enzyme-linked immunosorbent assay-based analytical protocol has often been referred to for the detection of LF in real samples. Signal amplification was accomplished using the streptavidin-biotin system. Here, an automated magnetic beads-based sandwich chemiluminescence enzyme immunoassay (MBs-sCLEIA) system was developed for the quantification of lactoferrin in pasteurized milk. The MBs-sCLEIA system consists of an automated chemiluminescence-based analyzer and a lactoferrin MBs-sCLEIA assay kit. Notably, our proposed method eliminates the need for pretreatment procedures and enables the direct addition of milk samples, allowing for the automatic quantitative detection of lactoferrin within a rapid 17 min timeframe for up to eight samples simultaneously. The MBs-sCLEIA was linear over the range of 7.24-800 ng/mL and displayed a limit of detection (LOD) of 2.85 ng/mL. As its good recovery and CV values indicate, the method exhibited high precision and accuracy. Furthermore, it was verified that it was selective towards five additional common milk proteins. A good correlation was observed between the results from the MBs-sCLEIA and heparin affinity column-HPLC (r2 = 0.99042), which proves to be a useful and practicable way of conducting an accurate analysis of lactoferrin in dairy products.
BACKGROUND: The carcinogenic transcription factor c-Myc is the most aggressive oncogene, which drive malignant transformation and dissemination of triple-negative breast cancer (TNBC). Recruitment of many cofactors, especially WDR5, a protein that nucleates H3K4me chromatin modifying complexes, play a pivotal role in regulating c-Myc-dependent gene transcription, a critical process for c-Myc signaling to function in a variety of biological and pathological contexts. For this reason, interrupting the interaction between c-Myc and the transcription cofactor WDR5 may become the most promising new strategy for treating c-Myc driven TNBC. METHODS: Immunoprecipitation and mass spectrometry (IP-MS) is used to screen proteins that bind c-Myc/WDR5 interactions. The interaction of METTL3 with c-Myc/WDR5 in breast cancer tissues and TNBC cells was detected by Co-IP and immunofluorescence. Subsequently, we further analyzed the influence of METTL3 expression on c-Myc/WDR5 protein expression and its interaction stability by Western blot and Co-IP. The correlation between METTL3 and c-Myc pathway was analyzed by ChIP-seq sequencing and METTL3 knockdown transcriptome data. The effect of METTL3 expression on c-Myc transcriptional activity was detected by ChIP-qPCR and Dual Luciferase Reporter. At the same time, the overexpression vector METTL3-MUT (m6A) was constructed, which mutated the methyltransferase active site (Aa395-398, DPPW/APPA), and further explored whether the interaction between METTL3 and c-Myc/WDR5 was independent of methyltransferase activity. In addition, we also detected the changes of METTL3 expression on TNBC's sensitivity to small molecule inhibitors such as JQ1 and OICR9429 by CCK8, Transwell and clonal formation assays. Finally, we further verified our conclusions in spontaneous tumor formation mouse MMTV-PyMT and nude mouse orthotopic transplantation tumor models. RESULTS: METTL3 was found to bind mainly to c-Myc/WDR5 protein in the nucleus. It enhances the stability of c-Myc/WDR5 interaction through its methyltransferase independent mechanism, thereby enhancing the transcriptional activity of c-Myc on downstream glucose metabolism genes. Notably, the study also confirmed that METTL3 can directly participate in the transcription of glucose metabolism genes as a transcription factor, and knockdown METTL3 enhances the drug sensitivity of breast cancer cells to small molecule inhibitors JQ1 and OICR9429. The study was further confirmed by spontaneous tumor formation mouse MMTV-PyMT and nude mouse orthotopic transplantation tumor models. CONCLUSION: METTL3 binds to the c-Myc/WDR5 protein complex and promotes glycolysis, which plays a powerful role in promoting TNBC progression. Our findings further broaden our understanding of the role and mechanism of action of METTL3, and may open up new therapeutic avenues for effective treatment of TNBC with high c-Myc expression.
Sex-specific behaviors are critical for reproduction and species survival. The sex-specifically spliced transcription factor fruitless (fru) helps establish male courtship behaviors in invertebrates. Forcing male-specific fru (fruM) splicing in Drosophila melanogaster females produces male-typical behaviors while disrupting female-specific behaviors. However, whether fru's joint role in specifying male and inhibiting female behaviors is conserved across species is unknown. We used CRISPR-Cas9 to force FruM expression in female Drosophila virilis, a species in which males and females produce sex-specific songs. In contrast to D. melanogaster, in which one fruM allele is sufficient to generate male behaviors in females, two alleles are needed in D. virilis females. D. virilis females expressing FruM maintain the ability to sing female-typical song as well as lay eggs, whereas D. melanogaster FruM females cannot lay eggs. These results reveal potential differences in fru function between divergent species and underscore the importance of studying diverse behaviors and species for understanding the genetic basis of sex differences.
Drosophila Proteins , Drosophila , Animals , Female , Male , Drosophila/genetics , Drosophila/metabolism , Drosophila melanogaster/genetics , Drosophila melanogaster/metabolism , Drosophila Proteins/genetics , Drosophila Proteins/metabolism , Courtship , Sexual Behavior, Animal , Nerve Tissue Proteins/metabolism , Transcription Factors/metabolism
Diosmin is a flavonoid derived from plants, possessing anti-inflammatory, antioxidant, antidiabetic, neuroprotective and cardiovascular protective properties. However, diosmin has low solubility in water, leading to low bioavailability. In this study, we constructed bilayer nanoparticles with trimethyl chitosan and soy peptides to improve the oral bioaccessibility and bioavailability of diosmin, and determined the characteristics and antioxidant properties of the diosmin-loaded nanoparticles. The results showed that the size of the nanoparticles was around 250 nm with the encapsulation efficiency higher than 97 %, and the nanoparticles were stable under regular conditions. In vitro digestion suggested the nanoparticles could protect diosmin from releasing in gastric digestion but promote the bioaccessibility of diosmin in intestine. Furthermore, the diosmin-loaded nanoparticles presented excellent antioxidant activities in vitro and significantly decreased the Lipopolysaccharides-induced brain Malondialdehyde (MDA) level by oral administration. Therefore, the reported nanoparticles may be an effective platform for improving the oral bioavailability of diosmin.
BACKGROUND: Human amniotic mesenchymal stem cells (hAMSCs) derived from amniotic membrane have multilineage differentiation, immunosuppressive, and anti-inflammation which makes them suitable for the treatment of various diseases. OBJECTIVE: This study aimed to explore the therapeutic effect and molecular mechanism of hAMSCs in ventricular remodeling (VR). METHODS: hAMSCs were characterized by a series of experiments such as flow cytometric analysis, immunofluorescence, differentiative induction and tumorigenicity. Mouse VR model was induced by isoproterenol (ISO) peritoneally, and the therapeutic effects and the potential mechanisms of hAMSCs transplantation were evaluated by echocardiography, carboxy fluorescein diacetate succinimidyl ester (CFSE) labeled cell tracing, histochemistry, qRT-PCR and western blot analysis. The co-culturing experiments were carried out for further exploring the mechanisms of hAMSCs-derived conditioned medium (CM) on macrophage polarization and fibroblast fibrosis in vitro. RESULTS: hAMSCs transplantation significantly alleviated ISO-induced VR including cardiac hypertrophy and fibrosis with the improvements of cardiac functions. CFSE labeled hAMSCs kept an undifferentiated state in heart, indicating that hAMSCs-mediated the improvement of ISO-induced VR might be related to their paracrine effects. hAMSCs markedly inhibited ISO-induced inflammation and fibrosis, seen as the increase of M2 macrophage infiltration and the expressions of CD206 and IL-10, and the decreases of CD86, iNOS, COL3 and αSMA expressions in heart, suggesting that hAMSCs transplantation promoted the polarization of M2 macrophages and inhibited the polarization of M1 macrophages. Mechanically, hAMSCs-derived CM significantly increased the expressions of CD206, IL-10, Arg-1 and reduced the expressions of iNOS and IL-6 in RAW264.7 macrophages in vitro. Interestingly, RAW264.7-CM remarkably promoted the expressions of anti-inflammatory factors such as IL-10, IDO, and COX2 in hAMSCs. Furthermore, the CM derived from hAMSCs pretreated with RAW264.7-CM markedly inhibited the expressions of fibrogenesis genes such as αSMA and COL3 in 3T3 cells. CONCLUSION: Our results demonstrated that hAMSCs effectively alleviated ISO-induced cardiac hypertrophy and fibrosis, and improved the cardiac functions in mice, and the underlying mechanisms might be related to inhibiting the inflammation and fibrosis during the ventricular remodeling through promoting the polarization of CD206hiIL-10hi macrophages in heart tissues. Our study strongly suggested that by taking the advantages of the potent immunosuppressive and anti-inflammatory effects, hAMSCs may provide an alternative therapeutic approach for prevention and treatment of VR clinically.
Fluoresceins , Interleukin-10 , Mesenchymal Stem Cells , Succinimides , Mice , Humans , Animals , Interleukin-10/pharmacology , Amnion , Isoproterenol , Ventricular Remodeling , Macrophages , Inflammation/chemically induced , Inflammation/therapy , Anti-Inflammatory Agents/therapeutic use , Anti-Inflammatory Agents/pharmacology , Fibrosis , Cardiomegaly
This study investigated the effects of microwave on preserving the quality of quinoa during storage. Quinoa treated with 9W/60s exhibited a significant decrease in fatty acid values compared to hot air treatment. Microwave effectively delayed lipid oxidation during quinoa storage by suppressing the increase in peroxide values. MDA gradually accumulated from peroxides during storage, reaching its peak at 0.423 µmol/L in the second week. Microwave disrupted the original hydrogen bonds in lipase, causing the unwinding of the α-helix and resulting in the loss of its regular structure. Microwave reduced the stability of the ß-sheet structure in lipoxygenase, breaking the natural secondary structure composition. The observed fluorescence and UV spectra features were similar, indicating that microwave alter the peptide chain of the enzyme's skeletal structure, increasing the exposure of hydrophobic chromophores. These results indicated the potential of microwave to enhance the stability of quinoa during storage.
Chenopodium quinoa , Chenopodium quinoa/chemistry , Microwaves , Peroxides , Fatty Acids
Background: Gastric cancer (GC) is the fourth most common cause of cancer-related death and the fifth most frequent malignant cancer, especially advanced GC. Carboxypeptidase X member 1 (CPXM1) is an epigenetic factor involved in many physiological processes, including osteoclast differentiation and adipogenesis. Several studies have shown the association of CPXM1 with multiple tumors; however, the mechanism of CPXM1 involvement in the progression of GC is yet to be characterized. Method: CPXM1 expression data were obtained from the Tumor Immune Estimation Resource. The Cancer Genome Atlas and the Gene Expression Omnibus databases were used to obtain patient-matched clinicopathological information, and the Kaplan-Meier plot database was utilized for the prognosis analysis of GC patients. The Catalog of Somatic Mutations in Cancer and cBioportal databases were adopted to study CPXM1 mutations in tumors. Next, we utilized the Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and Gene Set Enrichment Analysis for mechanism research. Furthermore, we performed tumor microenvironment and immune infiltration analysis based on CPXM1. Finally, we predicted sensitivity to several targeted drugs in GC patients based on CPXM1.CPXM1 is upregulated in GC and is correlated with poor prognosis, gender, and tumor stage in GC patients. Gene enrichment analysis suggested that CPXM1 may regulate the occurrence and progression of GC via the PI3K-AKT and TGF-ß pathway. Moreover, CPXM1 expression results in an increase in the proportion of immune and stromal cells. Additionally, the proportion of plasma cells was inversely related to the expression of CPXM1, whereas macrophage M2 expression was proportionate to CPXM1 expression. Finally, six small-molecule drugs that showed notable variations in IC50 between two groups were screened. Conclusion: These results suggested that CPXM1 regulates the progression of GC and may represent a novel target for the detection and treatment of GC.
In our previous study, a polyphenol-utilization targeted quinoa product was developed via solid-state fermentation with Monascus anka. In this study, we investigated the polyphenol-related novel functions of the fermented product further. Compared with unfermented quinoa, M. anka fermented quinoa alleviated the trapping effect of the macromolecules, especially in the colonic fermentation stage, resulting in enhanced polyphenol bioaccessibility. Lachnoclostridium, Megasphaera, Megamonas, Dialister, and Phascolarctobacterium might contribute to polyphenol liberation and metabolism in fermented quinoa. Additionally, fermented quinoa polyphenols presented an efficient anti-obesity effect by enhancing hepatic antioxidant enzyme activities, suppressing fatty acid synthesis, accelerating fatty acid oxidation, and improving bile acid synthesis. Moreover, fermented quinoa polyphenol supplementation alleviated gut microbiota disorder induced by a high-fat diet, resulting in a decreased ratio of Firmicutes/Bacteroidota, and increased relative abundances of Lactobacillus and Lachnoclostridium. The obtained results suggested that the principal anti-obesity effect of fermented quinoa polyphenols might act through the AMPK/PPARα/CPT-1 pathway. In conclusion, M. anka solid-state fermentation effectively enhanced the bioaccessibility of quinoa, and the fermented quinoa polyphenols showed considerable anti-obesity effect. Our findings provide new perspectives for the development of dietary polyphenol-based satiety-enhancing functional foods.
Chenopodium quinoa , Gastrointestinal Microbiome , Monascus , Polyphenols/pharmacology , Fermentation , Fatty Acids
Metabolic disorders, encompassing diabetes mellitus, cardiovascular diseases, gastrointestinal disorders, etc., pose a substantial global health threat, with rising morbidity and mortality rates. Addressing these disorders is crucial, as conventional drugs often come with high costs and adverse effects. This review explores the potential of royal jelly (RJ), a natural bee product rich in bioactive components, as an alternative strategy for managing metabolic diseases. RJ exhibits diverse therapeutic properties, including antimicrobial, estrogen-like, anti-inflammatory, hypotensive, anticancer, and antioxidant effects. This review's focus is on investigating how RJ and its components impact conditions like diabetes mellitus, cardiovascular disease, and gastrointestinal illnesses. Evidence suggests that RJ serves as a complementary treatment for various health issues, notably demonstrating cholesterol- and glucose-lowering effects in diabetic rats. Specific RJ-derived metabolites, such as 10-hydroxy-2-decenoic acid (10-HDA), also known as the "Queen bee acid," show promise in reducing insulin resistance and hyperglycemia. Recent research highlights RJ's role in modulating immune responses, enhancing anti-inflammatory cytokines, and suppressing key inflammatory mediators. Despite these promising findings, further research is needed to comprehensively understand the mechanisms underlying RJ's therapeutic effects.
Cardiovascular Diseases , Diabetes Mellitus, Experimental , Gastrointestinal Diseases , Metabolic Diseases , Rats , Animals , Bees , Diabetes Mellitus, Experimental/drug therapy , Fatty Acids/therapeutic use , Gastrointestinal Diseases/drug therapy , Metabolic Diseases/drug therapy , Cardiovascular Diseases/drug therapy , Anti-Inflammatory Agents/pharmacology , Anti-Inflammatory Agents/therapeutic use
Oat rice with great sensory acceptance was developed based on the combination method of milling and defatting (petroleum ether) treatment. In this study, the effect of milling and defatting treatment on the texture and digestion properties of oat rice was investigated. Results showed that milling and defatting treatment enhanced stickiness, enthalpy, and starch digestibility. The pasting temperature and hardness of oat rice were reduced. The lipid content of oat rice was significantly reduced by milling and defatting treatment, leading to a decrease in the formation of starch-lipid complex. Fourier transform infrared spectroscopy and X-ray diffraction analyses revealed that the application of milling and defatting treatments led to a reduction in the content of starch-lipid complexes in oats during the cooking process. Milling and defatting significantly enhanced both the rapid and slow digestion rates of oat rice. Specifically, the rapid digestion rate was found to be 2.5 times higher than the slow digestion rate. The nutritive components of oat rice were properly preserved, and the viscosity and elasticity of oat rice reached the maximum when milling for 40 s and defatting. This study provides a theoretical basis for oat products.
Cardiovascular disease is the deadliest disease in the world. Previous studies have shown that Dihydrotanshinone I (DHT) can improve cardiac function after myocardial injury. This study aimed to observe the protective effect and mechanism of DHT on H9c2 cells by establishing an oxygen-glucose deprivation/reoxygenation (OGD/R) injury model. By constructing OGD/R injury simulation of H9c2 cells in a myocardial injury model, the proliferation of H9c2 cells treated with DHT concentrations of 0.1 µmol/L were not affected at 24, 48, and 72 h. DHT can significantly reduce the apoptosis of H9c2 cells caused by OGD/R. Compared with the OGD/R group, DHT treatment significantly reduced the level of MDA and increased the level of SOD in cells. DHT treatment of cells can significantly reduce the levels of ROS and Superoxide in mitochondria in H9c2 cells caused by OGD/R and H2O2. DHT significantly reduced the phosphorylation levels of P38MAPK and ERK in H9c2 cells induced by OGD/R, and significantly increased the phosphorylation levels of AKT in H9c2 cells. DHT can significantly reduce the oxidative stress damage of H9c2 cells caused by H2O2 and OGD/R, thereby reducing the apoptosis of H9c2 cells. And this may be related to regulating the phosphorylation levels of AKT, ERK, and P38MAPK.
Furans , Hydrogen Peroxide , Phenanthrenes , Proto-Oncogene Proteins c-akt , Quinones , Animals , Proto-Oncogene Proteins c-akt/metabolism , Cell Line , Hydrogen Peroxide/metabolism , Signal Transduction , Oxygen/pharmacology , Oxygen/metabolism , Apoptosis , Glucose/metabolism , Myocytes, Cardiac/metabolism
AIMS: Inflammatory bowel disease (IBD) is a global disease. We aim to summarize the latest epidemiological patterns of IBD at the national, regional and global levels to give well-deserved attention and outline facilitating measures to reduce the disease burden. METHODS: We collected the incidence, prevalence, mortality and disability-adjusted life years (DALYs) of IBD in 204 countries and territories from 1990 to 2019 using data from the Global Burden of Disease Study 2019. We further calculated the estimated annual percentage change (EAPC) to qualify the temporal trends of IBD burden by sex, age and region over the past 30 years. RESULTS: Globally, a total of 404.55 thousand incident cases, 4898.56 thousand prevalent cases, 41.00 thousand deaths and 1622.50 thousand DALYs of IBD were estimated in 2019. The age-standardized DALYs decreased from 27.2 in 1990 to 20.15 per 100,000 people in 2019, with an EAPC of -1.04. The high socio-demographic index regions presented pronounced age-standardized rates (ASRs) consistently over the last 30 years. The high-income North America had the highest ASRs in 2019, followed by Western Europe and Australasia. No gender difference was observed after being stratified by sex. CONCLUSIONS: The accumulated IBD patients are expected to increase in the future due to the increased rate of IBD in developing countries, and social aging in developed countries. Understanding the changes in epidemiological patterns helps to provide evidence to mitigate the rising burden of IBD.
Global Burden of Disease , Inflammatory Bowel Diseases , Humans , Adult , Quality-Adjusted Life Years , Global Health , Prevalence , Inflammatory Bowel Diseases/epidemiology
