Background. Aplastic anaemia (AA) is a highly prevalent blood disorder in the East and Southeast Asian countries, and a proportion of the patients is poorly treated with immunosuppressive agents. This study is aimed at exploring the effects of sodium copper chlorophyllin (SCC) on rats with AA and at providing the theoretical basis for the treatment of AA using traditional Chinese medicine. Methods. A rat model of AA was induced by combining 5-fluorouracil with busulfan, and different groups were treated with 25mg/kg cyclosporin A (CsA) and low-, medium-, and high-dose SCC (25-, 50-, and 100-mg/kg; L-, M-, and H-SCC, respectively). A comparative analysis of peripheral blood counts, T-cell subsets, cytokine levels, bone marrow pathology, and APO-1 expression in mesenchymal stem cells in each group was conducted. Results. SCC can increase the platelet count and haemoglobin concentration in the peripheral blood of AA rats, whereas bone marrow biopsies revealed that the number of nucleated cells and megakaryocytes of SCC-treated rats increased compared with the model group. This was particularly evident in the H-SCC group. As regards the correction of immune function, unlike CsA, which reduced the absolute CD8+ T-cell count, SCC corrected the imbalanced CD4/CD8 ratio by increasing the absolute CD4+ T-cell count, whereas SCC increased the number of regulatory T-cells and reduced the level of interferon-γ in AA rats. When comparing the expression of APO-1 in the MSCs, results of the reverse-transcriptase polymerase chain reaction and Western blot analysis showed that SCC can increase the expression of APO-1 both at the mRNA and protein levels. Conclusion. We found that SCC can improve haematopoietic function and regress immune disorders in AA rats, which enhanced the expression of APO-1 in bone marrow MSCs. This may be one of the mechanisms of SCC in treating AA.

Background: Glioblastoma (GBM) is one of the most lethal tumors. Even though radiotherapy and chemotherapy have been greatly developed, the survival of patients with GBM is still only about 16 months. Methods: In this assay, centromere protein E (CENPE) expression levels were measured using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot (WB) assays. 5-ethynyl-2’-deoxyuridine (EDU) assay was used to assess the effect of CENPE on cell proliferation. The propidium iodide (PI) method was used to detect the cell cycle. Results: CENPE expression was increased in GBM tissues and was associated with clinical stage and unfavorable overall survival in glioma patients. Inhibition of CENPE expression resulted in proliferation inhibition of U251 and U87 cell. Cell cycle assay showed that CENPE mainly regulates the G0–G1 and G2/M phase transitions. Then, we found that CENPE regulated the proliferation of GBM mainly through WEE1 G2 checkpoint kinase (WEE1) pathway and can bind to WEE1. Conclusions: CENPE promotes GBM proliferation through WEE1 pathway and binding to WEE1.

Objective. To investigate the potential role of Momordica charantia polysaccharides (MCPs) in Parkinson’s disease (PD) and reveal the molecular mechanism of its function. Method. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium (1-methyl-4-phenylpyridinium, MPP+) were used to establish PD mice and cell models. The mice and cells were divided into 4 groups: Control group, Control+MCPs group, PD group, and PD+MCPs group. Pole climbing experiment and Rotarod experiment were used to observe the coordination ability of mice. High-performance liquid chromatography and enzyme-linked immunosorbent assay (ELISA) were used to determine neurotransmitters and metabolites, inflammatory factors TNF-α and IL-1β, oxidative stress-related markers SOD, MDA, and GSH in striatum tissues. Western blot was used to determine the protein levels of tyrosine hydroxylase (TH), oxidative stress-related protein Cytochrome C (Cytochrome C), and apoptosis-related proteins Bcl-2, Bax, and cleaved Caspase-3 in tissues and cells. Moreover, flow cytometry, PI staining, and fluorescence were used to observe cell apoptosis. Finally, the activation effect of MCPs on TLR4/MyD88/NF-κB signaling pathway was observed and verified. Results. Compared with the Control group, MPTP treatment can induce brain damage in mice (all $P<0.05$ ), change the metabolic state of neurotransmitters (all $P<0.05$ ), induce inflammation (all $P<0.05$ ), and induce apoptosis and the occurrence of oxidation reaction (all $P<0.05$ ); however, MCPs treatment can significantly reverse the above changes (all $P<0.05$ ). In cell models, studies have found that MCPs can play a protective role by regulating the activation state of TLR4/MyD88/NF-κB pathway. Conclusion. This study found that the application of MCPs therapy can play anti-inflammatory, antioxidative stress, and antiapoptotic effects in PD by regulating the activation of the TLR4/MyD88/NF-κB pathway.

Background: Cerebral ischemia-reperfusion injury (CIRI) is a major determinant of poor outcome after recanalization therapy in acute ischemic stroke. Microglial functional heterogeneity underpins neuroinflammation, yet the molecular mechanisms governing microglial phenotypic transitions remain incompletely understood. Metabolite-driven post-translational modifications (PTMs) have emerged as key regulators of microglial metabolism and inflammation, but whether PTM regulatory enzymes form co-expression modules that define microglial states is unknown. Methods: We analyzed single-cell RNA-seq datasets from five GEO studies (GSE174574, GSE227651, GSE245386, GSE267240, GSE319237) covering tMCAO reperfusion and permanent ischemia models. Microglia were purified using double filtration (P2ry12/Tmem119/Cx3cr1 ⁺ , Cd68/Adgre1/Ly6c ⁻ ). PTM enzyme co-expression modules were identified by non-negative matrix factorization (NMF). Spatiotemporal dynamics were assessed by module projection across timepoints (Sham, 1d, 3d, 7d) and pseudotime analysis. Independent validation was performed in an additional tMCAO dataset (GSE245386). Sex differences were explored in a mixed-sex permanent ischemia dataset (GSE267240). Results: Three robust PTM enzyme co-expression modules were identified: Metabolic stress-associated (M1), Pro-inflammatory-associated (M2), and Reparative-associated (M3). M1 was enriched in TCA cycle enzymes, M2 in inflammatory pathways (leukocyte activation, chemotaxis), and M3 in vascular development and translation. Module proportions and scores showed dynamic transitions: M1 decreased after reperfusion, M2 peaked at day 1-3, and M3 slightly increased at day 7. Independent validation in GSE245386 yielded high module conservation (cosine similarity = 0.874). Sex-specific differences in module distribution were observed in permanent ischemia (χ ² = 14.98, p = 0.00056). Conclusions: PTM enzyme co-expression modules delineate metabolic, pro-inflammatory, and reparative microglial states in CIRI with distinct spatiotemporal dynamics. This transcriptional framework supports the “PTM enzyme code” hypothesis and provides stage-specific targets for stroke therapy.