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Glioma poses a serious threat to human health and has a high mortality rate. Therefore, developing natural anti-tumour drugs for cancer treatment is an urgent priority. Schizophyllum commune is an edible and medicinal fungus, with polysaccharides as its main active components, which may have anti-tumour properties. Herein, we characterised S. commune fruiting body polysaccharides (SCFP) structure and evaluated its anti-glioma activity in vitro and in vivo. UV and FTIR spectra, high-performance gel chromatography, and monosaccharide composition analyses demonstrated that SCFP was a heteropolysaccharide with a molecular weight of 290.92 kDa. Among the monosaccharide compositions, mannose, galactose, and glucose were the most abundant. SCFP significantly inhibited the survival of the glioma cell lines U251 and U-87MG. U251 xenograft tumours treated with SCFP via gavage showed a 47.39 % inhibition, with no significant toxic side effects observed. SCFP upregulated aplasia Ras homologue member I (ARHI) expression, thereby regulating PI3K/AKT signalling, inhibiting tumour migration, and inducing apoptosis, to inhibit tumour growth. Furthermore, SCFP treatment increased the relative abundance of beneficial bacteria, including Akkermansia muciniphila, Ligilactobacillus murinus, and Parabacteroides goldsteinii, in tumour-bearing mice and restored the gut microbiota structure to that of the normal group (NG group) mice without tumours. Thus, SCFP has the potential for application as a natural anticancer drug., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. We declare that we do not have any commercial or related interests that conflict with our work., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Glioma is a serious primary malignant tumor of the human central nervous system with a poor prognosis and a high recurrence rate; however, inhibition of immune checkpoints can greatly improve the survival rate of patients. The purpose of this study was to investigate the regulation of PD-L1 by cordycepin and the mechanism of its anti-tumor action. The results of previous studies indicate that cordycepin has good anti-proliferative and anti-migratory activities and can induce apoptosis in U251 and T98G cells in vitro. Here, transcriptome sequencing showed that cordycepin may exert anti-tumor effects through the NOD-like receptor signaling pathway. Further intervention with BMS-1, a small molecule inhibitor of PD-L1, was used to explore whether inhibition of PD-L1 affected the regulation of the NOD-like receptor signaling pathway by cordycepin. Mechanistically, on the one hand, cordycepin regulated the expression of NFKB1 and STAT1 through the NOD-like receptor signaling pathway, thereby inhibiting the expression of PD-L1. In addition, inhibition of PD-L1 enhanced the regulation by cordycepin of the NOD-like receptor signaling pathway. On the other hand, cordycepin directly upregulated expression of STAT1 and downregulated that of PD-L1. In vivo studies further showed that cordycepin could downregulate expression of PD-L1 and NFKB1 and upregulate that of STAT1 in glioma xenograft tumor tissues, consistent with the results of in vitro studies. The results suggest that cordycepin may down-regulate the expression of PD-L1 through NOD-like receptor signaling pathway and NFKB signaling pathway, thereby inhibiting the immune escape of glioma, and can be developed as a PD-L1 inhibitor. Our results therefore provide a theoretical foundation for the use of cordycepin in treatment of glioma and enrich our understanding of its pharmacological mechanism., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)

Purpose: Glioblastoma is one of the malignant tumors with poor prognosis and no effective treatment is available at present., Methods: To study the effect of cordycepin combined with temozolomide on glioblastoma, we explored the effect of the combination based on network pharmacology and biological verification., Results: It was found that the drug combination significantly inhibited the cell growth, proliferation, migration and invasion of LN-229 cells. Drug combination inhibited epithelial-mesenchymal transition (EMT) by up-regulating the expression of E-cadherin and suppressing the expression of N-cadherin, Zeb1 and Twist1. Through network pharmacology, we further explored the molecular mechanism of drug combination against glioblastoma, and 36 drug-disease common targets were screened. The GO biological process analysis included 44 items (P < 0.01), which mainly involved the regulation of apoptosis, cell proliferation, cell migration, etc. The enrichment analysis of KEGG pathways included 28 pathways (P < 0.05), and the first four pathways were "MicroRNA in cancer, Proteoglycans in cancer, Pathways in cancer and PI3K-AKT signaling pathway". We detected the expression of important genes in the pathways and PPI network, and the results showed that the drug combination down-regulated NFKB1, MYC, MMP-9, MCL1, CTNNB1, and up-regulated PDCD4., Conclusion: Cordycepin combined with temozolomide may down-regulate MYC through "MicroRNA in cancer, Proteoglycans in cancer, Pathways in cancer and PI3K-AKT signaling pathway", which in turn regulate the expression of MCL1, CTNNB1, MMP9, PDCD4, thus regulating cell proliferation, migration and apoptosis in glioblastoma., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Objective: Pituitary abscess is an often misdiagnosed, rare clinical disorder. To improve diagnostic accuracy and the efficacy of surgical and antibiotic therapy for patients with pituitary abscess, herein, we retrospectively reviewed 15 patients who presented with pituitary abscesses from 2005 to 2022., Design: Retrospective study., Patients: Fifteen patients underwent transsphenoidal surgery and received antibiotic treatment., Measurements: Complete details regarding medical history, clinical manifestations, laboratory examinations, imaging studies, and treatment strategies were obtained for all patients., Results: Most patients presented with hypopituitarism and headaches, while some presented with fever, visual disturbances, and diabetes insipidus (DI). Abscesses showed significant annular enhancement post gadolinium injection. In most patients, pituitary abscess can be cured via microscopic or endoscopic drainage of the abscess followed by antibiotic treatment. Complete cure of pituitary abscess was observed in nine patients, with six cases of prolonged hypopituitarism and only one case of recurrence. Long-term hormone replacement therapy was effective in the postoperative management of hypopituitarism., Conclusions: The typical manifestations of pituitary abscess include hypopituitarism and headaches; the presence of an enhanced ring at the edge of the mass on contrast-enhanced magnetic resonance images (MRI) is highly suggestive of pituitary abscess. We recommend antibiotic treatment for 4-6 weeks postoperatively, based on the results of bacterial cultures or metagenomic next-generation sequencing (mNGS)., (Copyright © 2023 Elsevier Masson SAS. All rights reserved.)

Background: Glioblastoma is the most common and fatal primary malignant tumor in the central nervous system, and the prognosis is poor. Currently, there are no effective treatments for glioblastoma. Cordycepin is a natural active substance with significant anticancer activity and doxorubicin is a broad-spectrum anticancer drug. Cordycepin administered with doxorubicin is a potential drug combination for the treatment of glioblastoma. However, the mechanism of action for this drug combination has not yet been elucidated., Aim of the Study: To explore the complex mechanism of cordycepin combined with doxorubicin against glioblastoma using network pharmacology and biological verification., Materials and Methods: We used an MTT assay, colony formation assay, and scratch healing to detect the growth, proliferation, and migration of LN-229, U251 and T98G cells. Putative targets and the potential mechanism of action for the drug combination in glioblastoma were obtained through online databases, network construction, and enrichment analyses. We verified the expression of EMT-related genes and identified important therapeutic targets by western blot., Results: In this study, the combination of doxorubicin and cordycepin was found to significantly inhibit cell proliferation and migration and can induce apoptosis. These effects are better together than with either drug alone. The drug combination inhibited EMT by upregulating the expression of E-cadherin protein and downregulating the expression of N-cadherin, ZEB1, and Twist1 proteins. There were 71 potential targets for the drug combination in glioblastoma, and Kyoto Encyclopedia of Genes and Genome analysis suggested that the anticancer process may be mediated by proteoglycans in cancer, the tumor necrosis factor signaling pathway, microRNA in cancer, pathways in cancer, and other pathways. To study the molecular mechanism of anticancer activity, we detected the expression of target proteins with downregulated expression of NFKB1, MAPK8, MYC, and MMP-9 proteins and upregulated expression of cleaved caspase 3 that promoted the apoptosis of LN-229 cells., Conclusions: This study shows that the drug combination of doxorubicin and cordycepin effectively inhibits the growth and proliferation of LN-229 cells through multiple targets and multiple pathways, and the combination inhibits cell invasion and migration by regulating the EMT switch of tumor cells. Our findings provide new ideas about, and a theoretical basis for, the treatment of glioblastoma., Competing Interests: The authors declare that they have no competing interests., (© 2022 Chen et al.)