Prognostic marker CXCL5 in glioblastoma polyformis and its mechanism of immune invasion.

Glioblastoma multiforme (GBM) is the most aggressive brain cancer with a poor prognosis. Therefore, the correlative molecular markers and molecular mechanisms should be explored to assess the occurrence and treatment of glioma.WB and qPCR assays were used to detect the expression of CXCL5 in human GBM tissues. The relationship between CXCL5 expression and clinicopathological features was evaluated using logistic regression analysis, Wilcoxon symbolic rank test, and Kruskal-Wallis test. Univariate, multivariate Cox regression and Kaplan-Meier methods were used to assess CXCL5 and other prognostic factors of GBM. Gene set enrichment analysis (GSEA) was used to identify pathways associated with CXCL5. The correlation between CXCL5 and tumor immunoinfiltration was investigated using single sample gene set enrichment analysis (ssGSEA) of TCGA data. Cell experiments and mouse subcutaneous transplanted tumor models were used to evaluate the role of CXCL5 in GBM. WB, qPCR, immunofluorescence, and immunohistochemical assays showed that CXCL5 expression was increased in human GBM tissues. Furthermore, high CXCL5 expression was closely related to poor disease-specific survival and overall survival of GBM patients. The ssGSEA suggested that CXCL5 is closely related to the cell cycle and immune response through PPAR signaling pathway. GSEA also showed that CXCL5 expression was positively correlated with macrophage cell infiltration level and negatively correlated with cytotoxic cell infiltration level. CXCL5 may be associated with the prognosis and immunoinfiltration of GBM.

Predictive Value of Subdural Effusion Thickness for the Transformation of Post-Traumatic Subdural Effusion into Chronic Subdural Hematoma.

Objective: The primary aim of this research is to investigate the predictive value of subdural effusion thickness in determining the progression of post-traumatic subdural effusion to chronic subdural hematoma. Studying this progression is crucial as it helps in early diagnosis and effective management of chronic subdural hematoma, which is a serious and life-threatening condition. This research is valuable and relevant for improving patient outcomes and reducing the associated risks and complications. Methods: We conducted a retrospective examination of the clinical data obtained from 124 patients who were treated for post-traumatic subdural effusion at our neurosurgery department between March 2017 and March 2021. The data collection process involved reviewing the patients' medical records, radiographic images, and follow-up visits. We used strict criteria for patient selection, including a confirmed diagnosis of post-traumatic subdural effusion, availability of follow-up data, and no prior history of chronic subdural hematoma. Patients who experienced a progression of subdural effusion to chronic subdural hematoma were assigned to the hematoma group (26 cases). In comparison, those who did not show such progression were categorized into the effusion group (98 cases). We endeavored to identify potential risk factors contributing to the progression from subdural effusion to chronic subdural hematoma. The predictive strengths of these risk factors were evaluated using receiver operating characteristic (ROC) curves. Results: There were no statistically significant disparities between the two groups in terms of gender, hypertension, COPD, and GCS scores (P > .05). However, significant differences were noted in the variables of age, tSAH, the location of subdural effusion, and subdural effusion thickness (P < .05). Multivariate logistic regression analysis disclosed age (1.213), tSAH (12.542), and subdural effusion thickness (1.786) as independent risk factors for the conversion of TSE to CSDH (P < .05). The ROC curve showed the AUC values of age, tSAH, and subdural effusion thickness for predicting CSDH to be 0.739, 0.670, and 0.820, respectively, with a combined AUC value of 0.942, thereby outperforming the individual tests. Conclusion: In patients suffering from post-traumatic subdural effusion, the thickness of the subdural effusion emerges as a strong predictor for its progression into a chronic subdural hematoma. Clinicians should be particularly cautious when the effusion thickness exceeds 10.7 mm, as the likelihood of transformation increases significantly. These findings have important implications for clinical practice and patient management, highlighting the need for prompt and effective treatment to prevent chronic complications.

Resveratrol triggers autophagy-related apoptosis to inhibit the progression of colorectal cancer via inhibition of FOXQ1.

Colorectal cancer (CRC) is a significant health problem with elevated mortality rates, prompting intense exploration of its complex molecular mechanisms and innovative therapeutic avenues. Resveratrol (RSV), recognised for its anticancer effects through SIRT1 activation, is a promising candidate for CRC treatment. This study focuses on elucidating RSV's role in CRC progression, particularly its effect on autophagy-related apoptosis. Using bioinformatics, protein imprinting and immunohistochemistry, we established a direct correlation between FOXQ1 and adverse CRC prognosis. Comprehensive in vitro experiments confirmed RSV's ability to promote autophagy-related apoptosis in CRC cells. Plasmids for SIRT1 modulation were used to investigate underlying mechanisms. Molecular docking, glutathione-S-transferase pull-down experiments and immunoprecipitation highlighted RSV's direct activation of SIRT1, resulting in the inhibition of FOXQ1 expression. Downstream interventions identified ATG16L as a crucial autophagic target. In vivo and in vitro studies validated RSV's potential for CRC therapy through the SIRT1/FOXQ1/ATG16L pathway. This study establishes RSV's capacity to enhance autophagy-related cell apoptosis in CRC, positioning RSV as a prospective therapeutic agent for CRC within the SIRT1/FOXQ1/ATG16L pathway.

Ecological compensation in the Beijing-Tianjin-Hebei region based on ecosystem services flow.

Under a background of unbalanced regional economic development and ecological environments, the accurate identification of ecological compensation (EC) areas and the determination of compensation standards have become research key and hotspots. Their aim is to improve the long-term mechanisms of interregional EC. In this study, ecosystem services value (ESV) in the Beijing-Tianjin-Hebei region (BTH) in 2000, 2010 and 2019 are calculated using modelling and ecological economics methods. The region is divided into ecological output and input areas according to ecosystem services supply and demand. The breakpoint formula and field strength model are introduced to reveal the characteristics of ecosystem services flow (ESF) from output areas to input areas. By integrating a transfer correction coefficient system of natural, economic and social factors, an EC model based on ESF is constructed, and EC amounts for the BTH are calculated. The results are as follows: (1) The ESV of the BTH shows an increasing trend, with little change in spatial distribution characteristics. The high-value areas are distributed in the Taihang and Yanshan Mountains and Bashang Plateau in the northwest, while the low-value areas are concentrated in the Southeast Hebei Plain. (2) ESF mainly occurs in the western and northern regions of the BTH. Output areas are mainly distributed in the Taihang and Yanshan Mountains and Bashang Plateau, and their number is increasing. The flow radius, flow intensity and ESV transfer amounts also show increasing trends. (3) The ratio of EC paid by Beijing, Tianjin and Hebei is 1:0.2:2.56, the EC amounts are all provided to the Hebei Province, and the funds mainly flow to Chengde City, Zhangjiakou City and Baoding City. The proposed EC model based on ESF provides a basis and reference for the construction of an inter-regional EC mechanism in the BTH.

KIAA0101 knockdown inhibits glioma progression and glycolysis by inactivating the PI3K/AKT/mTOR pathway.

KIAA0101, a proliferating cell nuclear antigen (PCNA)-associated factor, is reported to be overexpressed and identified as an oncogene in several human malignancies. The purpose of this study is to determine the function and possible mechanism of KIAA0101 in glioma progression. KIAA0101 expression in glioma patients was analyzed by GSE50161 and GEPIA datasets. Kaplan-Meier survival analysis was used to evaluate the survival distributions. KIAA0101 expression in glioma cells were detected by qRT-PCR and western blot analyses. The function of KIAA0101 was investigated using MTT, flow cytometry, caspase-3 activity, and Transwell assays. Additionally, glycolytic flux was determined by measuring extracellular acidification rate (ECAR), glucose consumption, lactate production, and adenosine triphosphate (ATP) level. The changes of phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway were detected by western blot analysis. Results showed that KIAA0101 was upregulated in glioma tissues and cells. High KIAA0101 expression predicted a poor prognosis in glioma patients. KIAA0101 depletion impeded cell proliferation, migration, and invasion and triggered apoptosis in glioma cells. KIAA0101 silencing reduced the ECAR, glucose consumption, lactate production, and ATP level in glioma cells, suggesting that KIAA0101 knockdown inhibited glycolysis in glioma cells. Mechanistically, KIAA0101 knockdown inhibited the PI3K/AKT/mTOR pathway. In conclusion, KIAA0101 silencing inhibited glioma progression and glycolysis by inactivating the PI3K/AKT/mTOR pathway.

Cardamonin attenuates cerebral ischemia/reperfusion injury by activating the HIF-1α/VEGFA pathway.

Cardamonin is a chalcone with neuroprotective activity. The aim of our study was to explore the functions and mechanism of action of cardamonin in ischemic stroke. Oxygen-glucose deprivation and reperfusion (OGD/R)-induced human brain microvascular endothelial cells (HBMECs) and middle cerebral artery occlusion (MCAO) mouse model were utilized to mimic ischemic stroke. Cell viability was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide. Permeability was investigated via fluorescein isothiocyanate-dextran assay. Apoptosis was detected by TdT-Mediated dUTP Nick End Labeling staining. Hypoxia-inducible factor (HIF)-1α and vascular endothelial growth factor A (VEGFA) protein levels were measured using Western blotting. Brain injury was evaluated by 2,3,5-triphenyltetrazolium chloride staining, neurological score and brain water content. The 37 overlapping targets of ischemic stroke and cardamonin were predicted to be associated with the HIF-1/VEGFA signaling. Cardamonin alleviated OGD/R-induced viability reduction and increase of permeability and apoptosis in HBMECs. Cardamonin increased OGD/R-induced activation of the HIF-1α/VEGFA pathway. Inhibition of the HIF-1α/VEGFA signaling using inhibitor relieved the effect of cardamonin on cell viability, permeability and apoptosis in HBMECs under OGD/R. Cardamonin mitigated brain injury and promoted activation of the HIF-1α/VEGFA signaling in MCAO-treated mice. Overall, cardamonin protected against OGD/R-induced HBMEC damage and MACO-induced brain injury through activating the HIF-1α/VEGFA pathway.

Integrated Photoresponsive Alkaline Earth Metal Coordination Networks: Synthesis, Topology, Photochromism and Photoluminescence Investigation.

Photoresponsive materials are a key part of the age of smart technology that have potential in a broad range of applications. Coordination networks (CNs) are widely used due to their designability and stability. In this work, three novel alkaline earth metal coordination networks (AEM-CNs): [Mg(CMNDI)(H2 O)2 ], [Ca(CMNDI)(H2 O)2 ]⋅H2 O, and [Sr(CMNDI)(H2 O)(DMF)] with fsl, cds, and scn topology nets were synthetized via N,N'-bis(carboxymethyl)-1,4,5,8-naphthalenediimide (H2 CMNDI); the scn net is not found in the Reticular Chemistry Structure Resource or ToposPro. The reusable and sensitive photochromic properties of the three CNs enable them to be used as secret inks or ultraviolet detectors. In addition, the CNs also exhibited reusable photoluminescent turn-off toward the drug molecules, balsalazide disodium (Bal.) and colchicine (Col.), with good limits of detection of 0.16 and 0.70 µM. To the best of our knowledge, this is the first study of a fluorescence sensor for Bal. Thus, the AEM-CNs provide a design idea for integrated photoresponsive materials that could be further improved in the near future by further study.

Association Between the Polymorphism in miR-605 and Cancer Susceptibility: a PRISMA-Compliant Meta-Analysis.

Background: MicroRNAs (miRNAs) play important roles in cancer development. miR-605 was reported in several studies and showed potential as a prognostic biomarker. However, the association between miR-605 and the risk of cancer remained controversial in previous studies. Therefore, this meta-analysis was carried out to elaborate the association between polymorphism in miR-605 and cancer susceptibility. Methods: PubMed, Embase, Ovid Medline, and CNKI were searched for eligible studies through up to April 2018. The pooled odds ratios (ORs) with 95% confidence intervals (CIs) were derived from a random effects model. Statistical analysis was performed using STATA10.0 software or Review Manager 5.3 software. Results: A total of 8 eligible studies consisting of 2,462 cases and 3,716 controls were included in this meta-analysis. The ORs and 95% CIs in the 4 genetic models were (GA+GG vs. AA: OR = 0.97, 95% CI: 0.97, 1.19; GG vs. GA+AA: OR = 1.09, 95% CI: 0.81, 1.47; GG vs. AA: OR = 1.19, 95% CI: 0.77, 1.82; GA vs. AA: OR = 0.94, 95% CI: 0.77, 1.15). When stratified by cancer type and race, the results showed that polymorphism in miR-605 (rs2043556) is a protective factor for cancer in Asian population. But rs2043556 could increase the susceptibility of head and neck squamous cell carcinoma (NSCC) in the dominant genotype model. The results of subgroup analysis of race (Asian: GA+GG vs. AA: OR = 0.86, 95% CI: 0.75, 1.00; GA vs. AA: OR = 0.82, 95% CI: 0.72, 0.92) and of cancer type (NSCC: GA+GG vs. AA: OR = 1.36, 95% CI: 1.14, 1.61). Conclusions: The current meta-analysis demonstrated that the rs2043556 may decrease susceptibility in Asian populations, especially allelic-G may be a protective factor for cancer in carriers.

Dachengqi decoction alleviates acute lung injury by suppressing HIF-1α-mediated glycolysis.

ETHNOPHARMACOLOGICAL RELEVANCE: Acute lung injury (ALI) is an aggressive inflammatory disease of the lungs characterized by a high mortality rate. More and more researchers have found that herbal medicines are highly effective in preventing and treating inflammatory lung diseases. Among them, Dachengqi Decoction (DCQD) is considered to be the representative prescription of "lung-intestine combined treatment" in traditional Chinese medicine, and its potential protective mechanism against ALI is worthy of further study. AIM OF THE STUDY: Based on the theory of "lung-intestine combined treatment", the protective effect and molecular mechanism of DCQD in alleviating ALI were verified by network pharmacology and experiments. MATERIALS AND METHODS: The active ingredients of DCQD were obtained by UPLC-MS. Network pharmacology and molecular docking techniques were used to screen the active ingredient-target pathway of DCQD for ALI treatment. Additionally, the ALI model was constructed and verified in vivo according to the predicted results. RESULTS: 34 active components and 570 potential targets of DCQD were selected by network pharmacological analysis. In addition, 950 target genes of ALI and 2095 target genes related to sepsis were obtained, and 570 interlinked target genes of the two were identified. We finally screened out 199 common target genes critical to DCQD treatment of ALI and sepsis, and then enriched them with GO and KEGG. In the ALI model, studies have found that DCQD alleviates the inflammatory response of ALI, possibly by inhibiting HIF-1α-mediated glycolysis. CONCLUSION: This study confirmed the preventive effect of DCQD on ALI, and found that DCQD can improve the protective mechanism of ALI by regulating the expression of HIF-1α, down-regulating glycolysis and reducing inflammation.

Expression of miR-152 in cervical cancer and its influence on cisplatin resistance.

Background: Cervical cancer has a high mortality rate. Aim: We aimed to study the expression of micro ribonucleic acid 152 (miR-152) in cervical cancer and its influence on cisplatin (DDP) resistance. Methodology: Cervical cancer Hela cells were divided into control, DDP, DDP + mimic nc and DDP + miR-152 mimic groups. Results: DDP, DDP + mimic nc and DDP + miR-152 mimic groups had lower cell survival rate, smaller number of single clones and cells penetrating the membrane, and higher apoptosis rate and miR-152 expression than those of the control group (P<0.05). Compared with DDP and DDP + mimic nc groups, the cell survival rate, number of single clones and number of cells penetrating the membrane significantly decreased, while the apoptosis rate and miR-152 expression increased in the DDP + miR-152 mimic group (P<0.05). ERBB3 was a downstream target gene of miR-152. Hela cells transfected with miR-152 mimic had lower protein expressions of Snail, ERBB3, Akt2, p-Akt and c-myc than those of NC cells (P<0.05). Conclusion: MiR-152 suppresses the proliferation, migration and infiltration of cervical cancer cells and reduces their resistance to DDP chemotherapy by inhibiting the expressions of proteins in the ERBB3/Akt/c-myc and ERBB3/Akt/Snail pathways.

MiR-874-5p targets VDR/NLRP3 to reduce intestinal pyroptosis and improve intestinal barrier damage in sepsis.

BACKGROUND: Vitamin D receptor (VDR) is associated with intestinal barrier damage in sepsis. However, the mechanism of action of miR-874-5p/VDR/NLRP3 axis in disease has not been clearly explained. Therefore, the main content of this study is to explore the mechanism of this axis in intestinal barrier damage in sepsis. METHODS: In order to confirm the progress of miR-874-5p regulation of VDR/NLRP3 pathway and its involvement in intestinal barrier damage in sepsis, a series of molecular biology and cell biology methods were carried out in this study. These include the establishment of cecal ligation puncture model, Western blot, RT-qPCR, hematoxylin and eosin staining, double luciferase reporting method, Fluorescence in situ hybridization, immunohistochemistry, and enzyme-linked immunosorption assay. RESULTS: The expression level of miR-874-5p was higher and that of VDR was lower in sepsis. miR-874-5p was negatively correlated with VDR. Inhibition of miR-874-5p expression increased the expression of VDR, decreased the expression of NLRP3, reduced caspase-1 activation and IL-1ß secretion, reduced pyroptosis and inflammatory response, and thus protected the intestinal barrier damage in sepsis, all of which were reversed by the downregulation of VDR. CONCLUSIONS: This study suggested that down-regulation of miR-874-5p or up-regulation of VDR could reduce intestinal barrier damage in sepsis, which may provide potential biomarkers and therapeutic targets for intestinal barrier damage in sepsis.

[Effect of electroacupuncture on Treg/Th17 balance in spleen and serum inflammatory factors in obese mice].

OBJECTIVE: To observe the therapeutic effect of electroacupuncture(EA) on obese mice, and to explore the underlying mechanism of EA in treating obesity by focusing on the balance of regulatory T cells (Treg) and T helper 17 cells (Th17) and related inflammatory factors. METHODS: C57BL/6J male mice were randomly divided into normal group, model group and EA group, with 10 mice in each group. The obesity model was established by feeding the mice with high-fat diet. Mice in the EA group was treated with EA at "Zhongwan"(CV12), "Guanyuan"(CV4), "Zusanli"(ST36) and "Fenglong"(ST40) for 20 min every time, 3 times every week, for a total of 8 weeks. The food intake and body weight of mice were observed and recorded, and Lee's index was calculated; the contents of interleukin 2(IL-2), IL-4, IL-6, IL-10, IL-17A, gamma interferon (IFN-γ) and tumor necrosis factor(TNF)-α in serum were detected by multiplex liquid chip quantitative technique; the levels of Treg and Th17 cells in mice spleen tissues were detected by flow cytometry; and the expression levels of foxhead box p3(Foxp3) and retinoic acid related orphan receptor γt(ROR-γt) mRNA in spleen were detected by real-time quantitative PCR. RESULTS: Compared with the normal group, the food intake, body weight, Lee's index, the contents of IL-2, IL-6, IL-17A, IFN-γ and TNF-α in the serum, and the percentage of Th17 and expression of ROR-γt mRNA in the spleen tissues were significantly increased (P<0.01, P<0.001), while the contents of IL-4 and IL-10 in the serum, the percentage of Treg and expression of Foxp3 mRNA in the spleen tissues were significantly decreased (P<0.001, P<0.01) in the model group. Compared with the model group, the food intake, body weight, Lee's index, the contents of IL-2, IL-6, IL-17A, IFN-γ, and TNF-α in the serum, the percentage of Th17 and expression of ROR-γt mRNA in the spleen tissues were significantly decreased (P<0.01), while the contents of IL-4 and IL-10 in serum, the percentage of Treg and expression of Foxp3 mRNA in the spleen tissues were significantly increased(P<0.01, P<0.05) in the EA group. CONCLUSION: EA may improve the obese state of mice by regulating the balance of Treg/Th17 in spleen and the expression of inflammatory factors in serum.

Mechanism of Sijunzi Decoction in the treatment of colorectal cancer based on network pharmacology and experimental validation.

ETHNOPHARMACOLOGICAL RELEVANCE: Sijunzi Decoction（SJZD）, as a famous classical prescription for the treatment of colorectal cancer(CRC) in the traditional Chinese medicine (TCM), has achieved good curative effects in clinical practice. However, its specific ingredients and molecular mechanisms is still unclear. AIM OF THE STUDY: To analyze the effective ingredients and molecular mechanisms of SJZD in the treatment of CRC through network pharmacology technology and experimental validation. MATERIALS AND METHODS: First, the TCM Systems Pharmacology database and analysis platform database were searched to screen the effective chemical components of SJZD. Swiss Target Prediction was used to predict corresponding potential target genes of compounds. After that, we constructed a components and corresponding target network by Cytoscape. Simultaneously, 5 disease databases were used to search and filter CRC targets, and then we constructed a drug-disease target protein-protein interaction (PPI) network. Cytoscape 3.7 was used for visualization and cluster analysis, and Metascape database was used for GO and KEGG enrichment analysis. We drew the main pathway-target network diagram. Autodock vina1.5.6 was applied to molecular docking for the main compounds and target proteins. Subsequently, the potential mechanism of SJZD on colon cancer predicted by network pharmacological analysis was experimentally studied and verified in vivo and in vitro. RESULTS: 144 effective active chemical components, 897 potential targets, and 2584 CRC target genes were screened out. The number of common targets between the SJZD and CRC was 414.3250 GO biological process items and 186 KEGG signal pathways were obtained after analysis. The main compounds and the target protein had a good binding ability in molecular docking. The results of cell and animal experiments showed that SJZD could promote apoptosis and autophagy of CRC cells through PI3K/Akt/mTOR pathway. CONCLUSIONS: SJZD can treat CRC through multiple components, multiple targets and multiple pathways. We initially revealed the effective components and molecular mechanisms of SJZD in the treatment of CRC, and we used molecular docking and experiment for preliminary verification.

Oridonin promotes endoplasmic reticulum stress via TP53-repressed TCF4 transactivation in colorectal cancer.

BACKGROUND: The incidence of colorectal cancer and cancer death rate are increasing every year, and the affected population is becoming younger. Traditional Chinese medicine therapy has a unique effect in prolonging survival time and improving the prognosis of patients with colorectal cancer. Oridonin has been reported to have anti-cancer effects in a variety of tumors, but the exact mechanism remains to be investigated. METHODS: Cell Counting Kit-8 assay (CCK8) and 5-Ethynyl-2'-deoxyuridine (EdU) staining assay, Tranwell, and Wound healing assays were performed to measure cell proliferation, invasion, and migration capacities, respectively. The protein and mRNA expression levels of various molecules were reflected by Western blot and Reverse Transcription quantitative Polymerase Chain Reaction (qRT-PCR). Transcription Factor 4 (TCF4) and its target genes were analyzed by Position Weight Matrices (PWMs) software and the Gene Expression Omnibus (GEO) database. Immunofluorescence (IF) was performed to visualize the expression and position of Endoplasmic Reticulum (ER) stress biomarkers. The morphology of the ER was demonstrated by the ER tracker-red. Reactive Oxygen Species (ROS) levels were measured using a flow cytometer (FCM) or fluorescent staining. Calcium ion (Ca2+) concentration was quantified by Fluo-3 AM staining. Athymic nude mice were modeled with subcutaneous xenografts. RESULTS: Oridonin inhibited the proliferation, invasion, and migration of colorectal cancer, and this effect was weakened in a concentration-dependent manner by ER stress inhibitors. In addition, oridonin-induced colorectal tumor cells showed increased expression of ER stress biomarkers, loose morphology of ER, increased vesicles, and irregular shape. TCF4 was identified as a regulator of ER stress by PWMs software and GEO survival analysis. In vitro and in vivo experiments confirmed that TCF4 inhibited ER stress, reduced ROS production, and maintained Ca2+ homeostasis. In addition, oridonin also activated TP53 and inhibited TCF4 transactivation, further exacerbating the elevated ROS levels and calcium ion release in tumor cells and inhibiting tumorigenesis in colorectal cancer cells in vivo. CONCLUSIONS: Oridonin upregulated TP53, inhibited TCF4 transactivation, and induced ER stress dysregulation in tumor cells, promoting colorectal cancer cell death. Therefore, TCF4 may be one of the important nodes for tumor cells to regulate ER stress and maintain protein synthesis homeostasis. And the inhibition of the TP53/TCF4 axis plays a key role in the anti-cancer effects of oridonin.

Herba Patriniae and its component Isovitexin show anti-colorectal cancer effects by inducing apoptosis and cell-cycle arrest via p53 activation.

Colorectal cancer (CRC) is the most prevalent cancer of the digestive tract. Herba Patriniae (also known as Bai Jiang Cao, HP) have been widely used to manage diarrhea, ulcerative colitis, and several cancers, including CRC. Nonetheless, the molecular mechanisms underlying the pharmacological action of HP on CRC remain unclear. This study investigated the underlying mechanisms of HP against CRC using network pharmacology analysis and in vitro and in vivo experiments. The results revealed nine bioactive compounds of HP. Furthermore, 3460 CRC-related targets of the identified active compounds were predicted from the Gene Expression Omnibus (GEO) database. Furthermore, 65 common targets were identified through the intersection of two related targets. Moreover, ten hub genes, including CDK4, CDK2, CDK1, CCND1, CCNB1, CCNA2, MYC, E2F1, CHEK1, and CDKN1A were identified through the topological analysis. Meanwhile, the GO and KEGG pathway analysis revealed that the core target genes were majorly enriched in the p53 and HIF-1 signaling pathways. Moreover, HP promoted apoptosis and suppressed cell proliferation by activating the p53 signaling pathway in a dose-dependent manner, while a similar effect was observed for Isovitexin (the primary component of HP). Overall, this study provides valuable insights into the underlying mechanisms of HP and its component Isovitexin against CRC, providing a theoretical foundation for additional experimental verification of its clinical application.

Electroacupuncture ameliorates AOM/DSS-induced mice colorectal cancer by inhibiting inflammation and promoting autophagy via the SIRT1/miR-215/Atg14 axis.

Colorectal cancer (CRC) is one of the most common tumors of the digestive tract, with the third-highest incidence and the second-highest mortality rate among all malignant tumors worldwide. However, treatment options for CRC remain limited. As a complementary therapy, acupuncture or electro-acupuncture (EA) has been widely applied in the treatment of various inflammation-related diseases, such as obesity, ulcerative colitis and tumors. Although numerous pre-clinical and clinical studies have investigated the beneficial effects of acupuncture on CRC, the mechanism underlying the therapeutic action of EA is largely unknown. Evidence from previous studies has revealed that SIRT1 participates in CRC progression by activating autophagy-related miRNAs. Using azoxymethane/dextran sulfate sodium- (AOM/DSS-) induced colorectal cancer model in mice, we explored whether EA treatment can inhibit inflammation and promote autophagy via the SIRT1/miR-215/Atg14 axis. Our results showed that EA notably alleviated the CRC in mice, by decreasing the tumor number and DAI scores, inflammation, and increasing body weight of mice. Besides, EA increased the expression of SIRT1 and autophagy. Further experiments showed that SIRT1 overexpression downregulated miR-215, and promoted the expression of Atg14, whereas SIRT1 knockdown induced opposite results. In conclusion, EA can ameliorate AOM/DSS-induced CRC through regulating the SIRT1-mediated miR-215/Atg14 axis by suppressing inflammation and promoting autophagy in mice. These findings reveal a potential molecular mechanism underlying the anti-CRC effect of EA indicating that EA is a promising therapeutic candidate for CRC.

Research progress on acupuncture treatment in central nervous system diseases based on NLRP3 inflammasome in animal models.

Central nervous system (CNS) disorders exhibit complex neurophysiological and pathological mechanisms, which seriously affect the quality of life in patients. Acupuncture, widely accepted as complementary and alternative medicine, has been proven to exert significant therapeutic effects on CNS diseases. As a part of the innate immune system, NLRP3 inflammasome contributes to the pathogenesis of CNS diseases via regulating neuroinflammation. To further explore the mechanisms of acupuncture regulating NLRP3 inflammasome in CNS diseases, our study focused on the effects of acupuncture on neuroinflammation and the NLRP3 inflammasome in vascular dementia, Alzheimer's disease, stroke, depression, and spinal cord injury. This study confirmed that the activation of NLRP3 inflammasome promotes the development of CNS diseases, and inhibiting the activation of NLRP3 inflammasome is a potential key target for the treatment of CNS diseases. In addition, it is concluded that acupuncture alleviates neuroinflammation by inhibiting the activation of the NLRP3 inflammasome pathway, thereby improving the progression of CNS diseases, which provides a theoretical basis for acupuncture to attenuate neuroinflammation and improve CNS diseases.

Endoscopic surgery for intraventricular hemorrhage: A comparative study and single center surgical experience.

BACKGROUND: Intraventricular hemorrhage is a neurosurgical emergency, and a dangerous condition associated with high morbidity and mortality. Previously, hematoma evacuation is generally executed by external intracranial drainage (EVD) or surgical evacuation. Nowadays, endoscopic evacuation is emerging as a good alternative because it brings relatively less invasion and injury. However, successful endoscopic evacuation requires skilled manipulation of endoscopic devices and the evidence supporting its efficacy differs in different reports. AIM: To improve the technique usage and provide more evidence of endoscopic evacuation efficacy, we summarize our surgical experience and compared the outcomes of the endoscopic evacuation with EVD using real-world data. METHODS: We retrospectively studied 96 consecutive patients with intraventricular hemorrhage who underwent either endoscopic surgery (n = 43) or non-endoscopic surgery (n = 53) for hemorrhage evacuation between November 2013 and September 2019 in our center. Patients' conditions prior to and after the operation were evaluated and analyzed to assess the efficacy of the operation. The consciousness status improvement and perioperative in-hospital parameters in the two types of operation groups were assessed and compared. RESULTS: Patients in the endoscopic and non-endoscopic groups presented with a similar state of consciousness, with a comparable Glasgow Coma Scale (GCS) index. The average operation time of the endoscopic group was longer than that of the non-endoscopic group (median 2.42 h vs 1.08 h, P < 0.001). Although the endoscopic group was older and had a baseline Graeb score that indicated more severe hemorrhage than the non-endoscopic group (Graeb median: Endoscopic group = 9 vs non-endoscopic group = 8, P = 0.023), the clearance rate of hematoma was as high as 60.5%. Both the endoscopic and non-endoscopic groups showed an improved GCS index after surgery. However, this improvement was more marked in patients in the endoscopic group (median improvement of GCS index: Endoscope group = 4 vs non-endoscopic group = 1, P < 0.001). Additionally, the endoscopic group had a lower Graeb score than the non-endoscopic group after the operation. The intensive care unit stay of the endoscopic group was significantly shorter than that of the non-endoscopic group (median: endoscopic group = 6 d vs non-endoscope group = 7 d, P = 0.017). CONCLUSION: Endoscopic evacuation of intraventricular hemorrhage was generally an effective and efficient way for hemorrhage evacuation, and contributed remarkably to the improvement of consciousness in patients with intraventricular hemorrhage.

Facile Synthesis of TiO2/MoS2 Composites with Co-Exposed High-Energy Facets for Enhanced Photocatalytic Performance.

In this work, with the the H2TiO3 colloidal suspension and MoS2 as the precursors, TiO2/MoS2 composites composed of anatase TiO2 nanocrystals with co-exposed {101} and [111]-facets (nanorod and nanocuboid), {101} and {010} facets (nanospindle), and MoS2 microspheres constructed by layer-by-layer self-assembly of nanosheets were hydrothermally synthesized under different pH conditions. The characterization has been performed by combining X-ray powder diffraction (XRD), field emission scanning electron microscopy (FESEM), transmission electron microscopy (TEM), high resolution TEM (HRTEM), X-ray photoelectron spectroscopy (XPS), photoluminescence (PL) spectra, and UV-visible absorption spectrum analyses. The photocatalytic degradation of rhodamine B (RhB) in an aqueous suspension was employed to evaluate the photocatalytic activity of the as-prepared pHx-TiO2/MoS2 composites. The photocatalytic degradation efficiency of pH3.5-TiO2/MoS2 composite was the highest (99.70%), which was 11.24, 2.98, 1.48, 1.21, 1.09, 1.03, 1.10, and 1.14 times that of Blank, MoS2, CM-TiO2, pH1.5-TiO2/MoS2, pH5.5-TiO2/MoS2, pH7.5-TiO2/MoS2, pH9.5-TiO2/MoS2, pH11.5-TiO2/MoS2, respectively. The pH3.5-TiO2/MoS2 composite exhibited the highest photocatalytic degradation rate, which may be attributed to the synergistic effects of its large specific surface area, suitable heterojunction structure, and favorable photogenerated charge-separation efficiency. This work is expect to provide primary insights into the photocatalytic effect of TiO2/MoS2 composite with co-exposed high-energy facets, and make a contribution to designing more efficient and stable photocatalysts.

Integrated network pharmacology and experimental verification to investigate the mechanisms of YYFZBJS against colorectal cancer via CDK1/PI3K/Akt signaling.

Background: Colorectal cancer (CRC) is a common digestive tract malignancy with rising incidence and morbidity worldwide during recent years. Yi-Yi-Fu-Zi-Bai-Jiang-San (YYFZBJS), a traditional Chinese medicine formula, has showed positive effects against cancers. However, the mechanisms underlying its anticancer effects requires investigation. Methods: Information on bioactive compounds, potential YYFZBJS targets, and CRC-associated genes, was obtained from public databases. The key targets and ingredients as well their corresponding signaling pathways were identified using bioinformatic approaches, including Kyoto encyclopedia of genes and genomes (KEGG) analyses, gene ontology (GO), and protein-protein interaction (PPI). Subsequently, molecular docking was used to verify the main compounds-targets. Potential YYFZBJS therapeutic effects against CRC were validated in vitro and in vivo. Results: Using pharmacological network analysis, 40 YYFZBJS active compounds and 21 potential anti-CRC targets were identified. YYFZBJS was an important regulator of CRC through various targets and signaling pathways, particularly the cell cycle and PI3K/AKT pathway. Additionally, YYFZBJS suppressed the proliferation of CRC cells. Flow cytometry showed that YYFZBJS induced apoptosis and cell cycle arrest in the G2/M phase. Western blotting analysis indicated that YYFZBJS reduced the protein levels of CDK1, p-AKT, and p-PI3K, without altering total PI3K and AKT protein levels. In vivo analysis found that YYFZBJS inhibited tumor growth and PI3K/AKT signaling in a mouse model of CRC. Conclusion: As predicted by network pharmacology and validated by the experimental results, YYFZBJS inhibited proliferation, induced apoptosis and arrested cell cycle progression in CRC by modulating the CDK1/PI3K/Akt signaling pathway.