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This service exclusively searches for literature that cites resources. Please be aware that the total number of searchable documents is limited to those containing RRIDs and does not include all open-access literature.
Xiaoxuming decoction (XXMD) is a traditional Chinese herbal medicine (CHM) that is used for the treatment of stroke in China. Stroke injury damages the cerebral vasculature and disrupts the autoregulation of vasoconstriction and vasodilatation, which is crucial for maintaining constant cerebral blood flow (CBF). It has been reported that XXMD exerts a positive effect on cerebral circulation in animal models of stroke. However, the mechanisms underlying the regulatory effect of XXMD on vascular tone, and the interactions among the multiple components of XXMD, remain unclear. In this study, XXMD was found to induce relaxation of the basilar artery rings of rats precontracted by 5-hydroxytryptamine (5-HT) in vitro, in a dose-dependent manner. The modulation of vascular tone and the process of cerebral ischemia are mediated via the interactions between G protein-coupled receptors (GPCRs) and their ligands, including 5-HT, angiotensin II (Ang II), and urotensin II (UII). Thus, the potential synergistic effects of the different components of XXMD on the regulation of vasoconstriction and vasodilation were further investigated by molecular docking based on network pharmacology. We constructed and analyzed a database comprising 963 compounds of XXMD and studied the interactions between five vascular GPCRs (5-HT1A receptor (5-HT1AR), 5-HT1B receptor (5-HT1BR), Ang II type 1 receptor (AT1R), beta 2-adrenergic receptor (β2-AR), and UII receptor (UTR)) and the various herbal constituents of XXMD using molecular docking. By constructing and analyzing the compound-target networks of XXMD, we found that Glycyrrhizae Radix et Rhizoma, Ginseng Radix et Rhizoma, and Paeoniae Radix Alba were the three major herbs that contained a large number of compounds with high docking scores. We additionally observed that several constituents of XXMD, including gallotannin, liquiritin apioside, nariutin, 1,2,3,4,6-pentagalloylglucose, folic acid, and ginsenoside Rb1, targeted multiple vascular GPCRs. Moreover, the interactions between the components of XXMD and the targets related to vascular tone constituted the comprehensive cerebrovascular regulatory function of XXMD and provided a material basis of the vasoregulatory function of XXMD. The study reports the contributions of various components of XXMD to the regulatory effects on vascular tone and provides scientific evidence for the multicomponent and multitargeting characteristics of XXMD.
Geographic variability in esophageal cancer has been reported in China, but data are lacking at the local level. We aimed to investigate changes in disparities in esophageal cancer-related mortality among Chinese counties and whether county-level socioeconomic status was associated with this variation.
Tremella sanguinea is a traditional Chinese medicinal and edible mushroom. Polysaccharides from Tremella mushrooms have received increasing amounts of research attention due to their diverse pharmacological activities. In this study, via the incubation of basidiospores collected from fresh artificially cultivated basidiocarps of T. sanguinea, a haploid yeast strain of T. sanguinea was obtained, and it was found to be a typical loose-slime-forming yeast capable of producing a large amount of exopolysaccharides (EPS). Using DEAE-52 cellulose column chromatography and Sephadex G-100 gel permeation chromatography, the major polysaccharide, named TSPS-1, was separated and purified from the EPS produced by the haploid yeast strain of T. sanguinea. TSPS-1 was a homogeneous polysaccharide with a molecular weight of 2.5 × 103 kDa and consisted of rhamnose, glucose, xylose, mannose and glucuronic acid at a molar ratio of 1: 0.7: 62.2: 24.6: 11.5. The bioactivity of the TSPS-1 polysaccharide was evaluated. The results show that TSPS-1 exhibited noticeable antioxidant activity by scavenging hydroxyl radicals (EC50 = 1.92 mg/mL) and superoxide radicals (EC50 = 1.33 mg/mL), and prebiotic activity by promoting the growth of different probiotic strains in the genus Lactobacillus and Bifidobacterium. These results suggest that the cultivation of the haploid yeast strain can be a promising alternative for the efficient production of valuable T. sanguinea polysaccharides with antioxidant and prebiotic potential.
The impact of hepatitis B virus (HBV) infection on clinical outcomes of coronavirus disease 2019 (COVID-19) remains unclear. The aim of this study is to explore this impact. For this systematic review and meta-analysis, we searched PubMed, Web of Science, Embase, Cochrane library, China National Knowledge Infrastructure (CKNI), China Science and Technology Journal Database (VIP), and Wan Fang database for articles between 1 January 2020 and 1 February 2023. We used the Newcastle-Ottawa Quality Assessment to evaluate the study's quality. A random-effects meta-analysis was performed utilising the rates of severe/critical illness and death in COVID-19 patients with and without HBV infection. Eighteen studies with a total of 40,502 participants met the inclusion criteria. The meta-analysis showed that compared to those without HBV infection, COVID-19 patients with HBV were at increased risk of mortality (OR = 1.65, I2 = 58%, and 95% CI 1.08-2.53) and severity (OR = 1.90, I2 = 44%, and 95% CI 1.62-2.24). The region and gender may influence the outcomes of COVID-19 patients with HBV infection, but it requires more global data to confirm. In conclusion, HBV infection is significantly linked to an increased risk of severity and mortality in COVID-19.
Intestinal barrier dysfunction plays a central role in the pathological onset of Crohn's disease. We identify the cadherin superfamily member protocadherin 20 (PCDH20) as a crucial factor in Crohn's disease. Here we describe the function of PCDH20 and its mechanisms in gut homeostasis, barrier integrity, and Crohn's disease development.
Ribosomes are the workplace for protein biosynthesis. Protein production required for normal cell function is tightly linked to ribosome abundance. It is well known that ribosomal genes are actively transcribed and ribosomal messenger RNAs (mRNAs) are rapidly translated, and yet ribosomal proteins have relatively long half-lives. These observations raise questions as to how homeostasis of ribosomal proteins is controlled. Here, we show that ribosomal proteins, while posttranslationally stable, are subject to high-level cotranslational protein degradation (CTPD) except for those synthesized as ubiquitin (Ub) fusion precursors. The N-terminal Ub moiety protects fused ribosomal proteins from CTPD. We further demonstrate that cotranslational folding efficiency and expression level are two critical factors determining CTPD of ribosomal proteins. Different from canonical posttranslational degradation, we found that CTPD of all the ribosomal proteins tested in this study does not require prior ubiquitylation. This work provides insights into the regulation of ribosomal protein homeostasis and furthers our understanding of the mechanism and biological significance of CTPD.
This study reported the isolation and identification of bioactive compounds from Dioscorea nipponica Makino, a plant used in traditional medicine for various ailments. Nine compounds were isolated, including a new compound named as diosniposide E, which was elucidated by analyzing its 1H-NMR, 13C-NMR, DEPT, COSY, HMBC and MS data and comparing them with data available in literature. The other eight compounds were identified as known compounds. Theoretical calculations of energy and the generation of a molecular electrostatic potential surface map were employed to assess the antioxidant capacity of nine compounds, the calculation results exhibited that compounds 5 and 6 had strong antioxidant capacities. To further evaluate the antioxidant activities of the investigated compounds, the DPPH and ABTS assays were conducted. The results from the DPPH scavenging activity test revealed that compounds 4-6 exhibited enhanced scavenging activities compared to L-ascorbic acid, while displaying similar efficacy to trolox. Moreover, the ABTS scavenging activities of compounds 4-6 were found to surpass those of L-ascorbic acid and trolox. In terms of α-glucosidase inhibition, compounds 3 and 4 displayed remarkable inhibitory activities that surpassed the effects of acarbose. Additionally, compound 2 exhibited potent anticholinesterase activities, outperforming donepezil. This research provides insights into the potential bioactive compounds present in Dioscorea nipponica Makino and may contribute to its use in traditional medicine.
Salmonella, a prevalent foodborne pathogen, poses a significant social and economic strain on both food safety and public health. The application of phages in the control of foodborne pathogens represents an emerging research area. In this study, Salmonella pullorum phage vB_SpuM_X5 (phage X5) was isolated from chicken farm sewage samples. The results revealed that phage X5 is a novel Myoviridae phage. Phage X5 has adequate temperature tolerance (28 °C-60 °C), pH stability (4-12), and a broad host range of Salmonella bacteria (87.50% of tested strains). The addition of phage X5 (MOI of 100 and 1000) to milk inoculated with Salmonella reduced the number of Salmonella by 0.72 to 0.93 log10 CFU/mL and 0.66 to 1.06 log10 CFU/mL at 4 °C and 25 °C, respectively. The addition of phage X5 (MOI of 100 and 1000) to chicken breast inoculated with Salmonella reduced bacterial numbers by 1.13 to 2.42 log10 CFU/mL and 0.81 to 1.25 log10 CFU/mL at 4 °C and 25 °C, respectively. Phage X5 has bactericidal activity against Salmonella and can be used as a potential biological bacteriostatic agent to remove mature biofilms of Salmonella or for the prevention and control of Salmonella.
Regulator of G protein signaling 1 (RGS1) is known to be highly expressed in various tumors, but its specific effects and regulatory mechanism in ovarian cancer (OC) progression are not well understood. To delve into the tumor biology, a predictive risk model for OC was developed, incorporating RGS1, PRKG2, CD24, and ABCB1, with RGS1 exhibiting the strongest correlation. The model's reliability and validity were confirmed through Kaplan-Meier analysis, receiver operating characteristic (ROC) curve, and principal component analysis (PCA). The risk score was validated as an independent indicator of overall survival, and a nomogram model was created to predict overall survival. Moreover, RGS1 expression was found to be up-regulated and associated with a poor prognosis in OC. Functional studies revealed that deleting RGS1 inhibited OC cell proliferation both in vitro and in vivo, while overexpression of RGS1 enhanced cell proliferation. Additionally, blocking the NF-kB pathway was shown to impede RGS1-induced proliferation, and overexpression of p65 partially reversed the effects of RGS1 deletion, promoting the tumorigenic properties of OC cells. These findings suggest that RGS1 could be a valuable biomarker for predicting prognosis and a potential novel therapeutic target for OC treatment.
While fructose is a key dietary component, concerns have been raised about its potential risks to the liver. This study aimed to assess quercetin's protective effects against fructose-induced mouse hepatic steatosis. Thirty-two male C57BL/6J mice were randomly allocated into four groups: control, high fructose diet (HFrD), HFrD supplemented with low-dose quercetin (HFrD+LQ), and HFrD supplemented with high-dose quercetin (HFrD+HQ). Biochemical, pathological, immune, and metabolic parameters were assessed. Quercetin treatment significantly reduced liver fat percentages in mice on a high fructose diet, with the most notable reduction observed in the HFrD+HQ group. Histological examination confirmed this reduction, revealing diminished lipid droplets and decreased inflammation and steatosis in hepatocytes. Compared to the high fructose group, interleukin-1 β and tumor necrosis factor alpha were significantly decreased, serum aspartate aminotransferase concentrations were markedly reduced, and blood high-density lipoprotein concentrations were substantially elevated after quercetin intervention (p < 0.05). Total bilirubin and triglyceride levels, which were significantly altered following high fructose intervention and reversed after quercetin intervention. Following the administration of 100 mg/kg quercetin, the Firmicutes/Bacteroidetes ratio was significantly reduced compared to the high fructose group. At the genus level, Erysipelotrichaceae_uncultured, Faecalibaculum, Odoribacter, and Allobaculum were significantly decreased (p < 0.05), Lacnospiraceae NK4A136 group, Parabacteroides, and Alloprevotella significantly increased (p < 0.05). However, the 50 mg/kg quercetin treatment only decreased the abundance of Erysipelotrichaceae_uncultured (p < 0.05). In addition, quercetin significantly enhanced the content of propionic acid and total acid (p < 0.05). Moreover, the intestinal flora showed a significant correlation with the hepatic health-related phenotype in mice. Both 50 and 100 mg/kg quercetin treatments significantly mitigated liver fat deposition in mice with fructose-induced hepatic steatosis. However, the higher dose of quercetin (100 mg/kg) demonstrated a more pronounced effect in reducing liver inflammation, likely due to its impact on gut microbiota regulation. This suggests quercetin's potential as a therapeutic agent for fructose-related hepatic steatosis, emphasizing the importance of dose considerations.
Psoriasis is a chronic inflammatory skin disorder characterized by hyperproliferation of keratinocytes and persistent inflammation. Although persistent activation of signal transducer and activator of transcription 3 (STAT3) is implicated in its pathogenesis, the mechanisms underlying the sustained STAT3 activation remain poorly understood. Here, we identify sphingosine-1-phosphate receptor 3 (S1PR3) as a critical regulator of STAT3 activation and psoriasis pathogenesis, orchestrating a self-amplifying circuit that sustains keratinocyte hyperproliferation and chronic inflammation. S1PR3 expression is markedly elevated in psoriatic lesions and correlates with disease severity. Using genetic and pharmacological approaches, we reveal a novel S1PR3-Src-STAT3 signaling axis that drives both early and prolonged STAT3 activation in keratinocytes. Mechanistically, S1PR3 operates through Gαi/PKA-mediated Src activation, enhancing STAT3 phosphorylation and subsequent transcriptional activity. Importantly, we reveal a previously unrecognized positive feedback loop wherein activated STAT3 directly upregulates S1PR3 expression, perpetuating inflammation and hyperproliferation. Genetic deletion of S1pr3 in mice or pharmacological inhibition of S1PR3 significantly attenuates psoriasis-like skin inflammation, decreasing epidermal hyperplasia, dermal angiogenesis, and inflammatory mediator production. These findings provide new insights into the molecular mechanisms underlying psoriasis and identify S1PR3 as a promising therapeutic target. Our study suggests that disrupting the S1PR3-STAT3 feedback loop may offer a novel strategy for treating psoriasis and potentially other chronic inflammatory diseases driven by persistent STAT3 activation.
The purpose of this study was to investigate the relationships between a Power Leg Press test (PLP) with walking capacity and self-reported performance and participation in individuals with Cerebral Palsy (CP), and to compare the strength of the associations between two power tests (PLP and isokinetic (IsoK)) with walking capacity.
Colon adenocarcinoma (COAD), a common digestive system malignancy, involves crucial alterations in mitochondria-related genes influencing tumor growth, metastasis, and immune evasion. Despite limited studies on prognostic models for these genes in COAD, we established a mitochondrial-related risk prognostic model, including nine genes based on available TCGA and MitoCarta 3.0 databases, and validated its predictive power. We investigated the tumor microenvironment (TME), immune cell infiltration, complex cell communication, tumor mutation burden, and drug sensitivity of COAD patients using R language, CellChat, and additional bioinformatic tools from single-cell and bulk-tissue sequencing data. The risk model revealed significant differences in immune cell infiltration between high-risk and low-risk groups, with the strongest correlation found between tissue stem cells and macrophages in COAD. The risk score exhibited a robust correlation with TME signature genes and immune checkpoint molecules. Integrating the risk score with the immune score, microsatellite status, or TMB through TIDE analysis enhanced the accuracy of predicting immunotherapy benefits. Predicted drug efficacy offered options for both high- and low-risk group patients. Our study established a novel mitochondrial-related nine-gene prognostic signature, providing insights for prognostic assessment and clinical decision-making in COAD patients.
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