Suiping Huang

Background: Matrine and oxymatrine are bioactive alkaloids from Sophora species with reported anti-inflammatory and antioxidant effects in ulcerative colitis (UC). However, their overall efficacy has not been systematically evaluated. Methods: Databases including PubMed, EMBASE, Web of Science, Scopus, CNKI, Wanfang, VIP, and SinoMed were searched to January 2026. Animal studies using matrine or oxymatrine monotherapy in UC models were included. Effect sizes were calculated as standardized mean differences (SMDs) with 95% confidence intervals (CIs). Results: Thirteen studies were included. Compared with controls, matrine-type alkaloids significantly reduced histopathological scores (SMD = −3.47, 95% CI: −4.83 to −2.11) and decreased Disease Activity Index (DAI) at 3 days (SMD = −2.92, 95% CI: −4.27 to −1.57) and 7 days (SMD = −4.76, 95% CI: −6.30 to −3.23), but not at 14 days (SMD = −1.01, 95% CI: −2.22 to 0.20). Body weight increased at 7 days (SMD = 2.76, 95% CI: 1.95–3.57) and 14 days (SMD = 2.41, 95% CI: 0.12–4.69), and colon length was also increased (SMD = 2.09, 95% CI: 1.55–2.64). Matrine-type alkaloids reduced TNF-α (SMD = −2.88, 95% CI: −3.50 to −2.26), IL-6 (SMD = −2.91, 95% CI: −4.64 to −1.17), IL-1β (SMD = −2.73, 95% CI: −4.27 to −1.19), and MDA levels (SMD = −3.06, 95% CI: −4.47 to −1.65), while increasing SOD activity (SMD = 2.63, 95% CI: 1.37–3.89). Subgroup analyses suggested generally similar directions of effect across species and model types. The pooled effect estimate appeared larger in the oxymatrine subgroup than in the matrine subgroup, but this indirect comparison should be interpreted cautiously. Conclusion: Matrine-type alkaloids may exert protective effects in UC animal models by improving histological damage, reducing disease activity, and modulating inflammatory and oxidative stress pathways. These findings suggest their potential as multi-target therapeutic agents, although further high-quality studies are required for clinical translation. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD420261376235 , identifier CRD420261376235.

CGB5 plays an important factor in numerous different cancers and is strongly associated with patient prognosis. Unfortunately, there is currently no data, however, on whether CGB5 plays a role in pan-cancer diseases. Research on CGB5 in pan-cancer has been conducted through multiple websites and public databases, including TCGA, HPA, UALCAN, cbiopportal Platform, UALCAN, GSCA, Kaplan-Meier Plotter, TIMER, TISIDB, SangerBox Website, and metscape. The genomic, transcriptomic, epigenetic, immune microenvironmental, and clinical prognostic significance of CGB5 across pan-cancer is investigated with the resulting outcome. CGB5 expression in gastric cancer was further detected, and the potential mechanism of its influence on prognosis was elucidated. This study found that abnormal CGB5 expression in pan carcinoma is correlated with a poorer prognosis. Aberrant CGB5 expression is potentially linked to gene mutations, copy number variation (CNV), and DNA methylation. In addition, this study revealed a robust association between the expression of CGB5 and immune cell infiltration across various types of cancer, with differences in cell type and level among distinct tumor types. In addition, the present investigation has shown that A strong association has been detected between the upregulation of CGB5 expression and immune cell infiltration in various forms of cancer, with differences in the different tumor types in the type and level of immune cell infiltration. Our further cell experiments also confirmed the upregulation of CGB5 within the context of gastric cancer. In conclusion, it has been noted that CGB5 expression exhibited a substantial rise across wide types of malignancies, and this upregulation was shown to exhibit a significant association with the prognosis of individuals who have cancer. Further studies showed that CGB5 expression in tumors affects the tumor immune microenvironment and promotes tumorigenesis. We also explored CGB5 expression in gastric cancer and clarified its potential prognostic mechanism. It reveals CGB5's significance in cancer diagnosis and treatment.

Background: Liver hepatocellular carcinoma (LIHC) is a complicated disease with poor survival and lack of viable treatment options. The roles of ferroptosis and immunotherapy in LIHC are increasingly prominent, but the interplay of ferroptosis with the tumor microenvironment (TME) in LIHC is currently under-investigated.Methods: In this study, we analyzed normal liver tissues and tumor tissues from the TCGA and GTEx databases to obtain differentially expressed ferroptosis-related genes (FRGs). We then clustered LIHC based on the expression levels of selected FRGs and acquired distinct subtypes with significant heterogeneity regarding survival prognoses, PD-L1 expression, and immune cell infiltration. The correlation of those FRGs with TME in LIHC and pan-cancer analysis was also investigated. GO functional annotations and KEGG pathway analyses were performed to investigate the potential reactions of the obtained differentially expressed genes (DEGs). Further external validation was performed using microarrays on the GEO database and the key ferroptosis regulator SLC7A11 expression between LIHC and normal cells was detected by Western blotting.Results: A large proportion of genes were upregulated in the LIHC group. Among three clusters, cluster 3 had the worst prognosis combined with the highest PD-L1 expression and was positively correlated with various immune cells. Subsequently, survival analysis and Cox regression analysis screened out SLC7A11 as an independent prognostic factor in LIHC featured strong PD-L1 expression and unfavorable survival time. We filter out SLC7A11 as an independent prognostic signature in LIHC patients with strongly associated PD-L1 expression and unfavorable survival probability. In the pan-cancer analysis, high expression of SLC7A11 showed poor overall survival in seven cancers, while the correlation between immune checkpoints (ICs) and SLC7A11 varied by cancer type, indicating the potential therapeutic effects of SLC7A11 in cancers other than LIHC. Western blot was further employed to verify the expression of SLC7A11 in LIHC in vitro.Conclusion: Ferroptosis and TME synergistically play key roles in oncogenesis and progression of LIHC, and SLC7A11 can be used as a predictive biomarker for customized immunotherapy.

Inhibin subunit beta B (INHBB) is a potential prognostic biomarker for a variety of cancers. However, its role in gastric cancer (GC) remains elusive. The differential expression data of INHBB in tumor and normal tissues were extracted from several databases and genetic alterations of INHBB were assessed by cBioPortal. Kaplan-Meier analysis was used to evaluate the survival rate of patients with GC with INHBB and association with clinical features in GC. Cox regression analysis was used to explore the prognostic value of clinical indicators and INHBB in GC, and a nomogram prognostic model was established. In addition, the predictive validity of the nomogram model was assessed by time-depended receiver operating characteristic (ROC) and calibration curves. Functional enrichment analyses were conducted to functionally annotate INHBB. Notably, we found that the quantitative assessment of immune cell subpopulation infiltration correlated with INHBB expression. INHBB expression is upregulated in GC and is correlated with several clinical features including prognostic indicators and a histological type. Genetic alterations were observed in INHBB, its DNA methylation level was negatively correlated with INHBB expression. High INHBB expression is associated with a poor prognosis and is an independent risk factor for prognosis in GC, along with age and residual tumor. The nomogram model showed a good prediction ability and was validated by time-depended ROC and calibration curves. Functional enrichment analysis indicated that INHBB-associated genes were enriched in tumor microenvironment Gene Ontology (GO) terms and were correlated with tumor-associated pathways. INHBB has a regulatory function in immune cell infiltration, especially macrophage infiltration in GC. Specifically, patients with GC with high INHBB expression and high macrophage infiltration have a worse prognosis. INHBB expression was negatively correlated with the expression of chemokines/chemokine receptors and plays a regulatory role in immunoinhibitor/immunostimulator-involved pathways. INHBB is a potential prognostic biomarker for GC and may drive the abnormal activity of critical cancer-associated pathways, potentially contributing to immune cell infiltration to promote GC development.

Several gastrointestinal phenotypes and impairment of duodenal mucosal barrier have been reported in clinical studies in patients with functional dyspepsia (FD). Due to the preferential colonization of the mucosa, intestinal microbes and their metabolites are commonly involved in host metabolism and immune responses. However, there are no studies on the intertwined correlation among multi-level data. For more comprehensive illustrating, a multi-omics analysis focusing on the duodenum was performed in the FD rat model. We found that differential microbiomes in the duodenum were significantly correlated with the biosynthesis of lipopolysaccharide and peptidoglycan. The innate immune response-related genes, which were upregulated in the duodenum, were associated with the TLR2/TLR4-NFκB signaling pathway. More importantly, arachidonyl ethanolamide (anandamide, AEA) and endocannabinoid analogues showed linear relationships with the FD phenotypes. Taken together, multi-level data from microbiome, transcriptome and metabolome reveal that AEA may regulate duodenal low-grade inflammation in FD. These results suggest an important cue of gut microbiome–endocannabinoid system axis in the pathogenesis of FD.

Background: Inhibin subunit beta A (INHBA) is reportedly a potential prognostic biomarker for a variety of cancers. However, its role in gastric cancer (GC) remains elusive. Methods: The expression of INHBA in GC and healthy tissues based on the data obtained from the UCSC Xena database. Logistic regression and Cox regression was performed to explore the correlation between clinical indicators and INHBA expression. Kaplan–Meier curve analysis was performed to assess the impact of INHBA expression on overall survival(OS). In addition, Received operating characteristic curve analysis was implied to clarify the diagnostic role of INHBA in GC. Functional analyses were conducted to explain the potential functions and enrichment pathways for INHBA. TIMER and GEPIA databases were used to calculate the confidence between INHBA and immune cell infiltration in GC. Results: INHBA was upregulated in GC(P < 0.001) and associated with a poor prognosis(P = 0.037). INHBA expression was an independent risk factor for OS(P = 0.004). Additionally, INHBA was a potential diagnostic marker in GC(AUC=0.961) and it was associated with extracellular matrix organization, response to growth factor, and cell-substrate adhesion. Tumor-associated signaling pathways, such as Wnt, Hippo, and p53, were associated with INHBA. Reactome pathways, such as collagen formation and extracellular matrix organization, were significantly enriched. Moreover, high INHBA expression displayed a strong correlation with immune cell infiltration, especially with macrophage infiltration in GC.Conclusions: INHBA could be a potential prognostic biomarker for GC and may drive the abnormal activity of critical cancer-associated pathways, potentially contributing to immune cell infiltration to promote GC development and becoming a new drug target for targeted GC therapies.

Purpose: Banxia xiexin decoction (BXXX) is a classical Chinese herbal compound for the treatment of gastrointestinal diseases. Its ingredients are also considered helpful for cancer rehabilitation. Here, we will explore the regulatory mechanism of BXXX acting on PD-L1 in gastric cancer (GC). Methods: GC samples and the general baseline data of the patients were collated. Immunohistochemical (IHC) detected the expression of programmed cell death-ligand 1(PD-L1), hypoxia-inducible factor-1 (HIF-1), epidermal growth factor receptor (EGFR), interferon-γ receptor (IFNGR) and Toll-like receptor 4 (TLR4). ELISA detected the expressions of EGF, IFNG and IL-6 in serum samples. Network tools were used to analyze the potential molecules of BXXX. In the cell experiment, CCK-8 detected the cell proliferation. Tunel detected the apoptosis. Western blot detected the expression of related proteins. In animal experiments, the tumor volume of GC-bearing mice was observed. Expression of EGF, IFNG and IL-6 in the serum of tumor-bearing GC mice were detected by ELISA. Western blot detected the expression of related proteins. Results: The expressions of PD-L1, HIF-1, EGFR, IFNGR and TLR4 in the tissues of GC patients were significantly increased, and the expressions of EGF, IFNG and IL-6 in serum were increased. The molecular results of the network tools showed that BXXX and its main components have a targeting effect on the key molecules of each pathway in the PD-L1 regulatory network. Cell experiments showed that BXXX can inhibit the expression of PD-L1, HIF-1, EGFR and TLR4, but has no significant effect on the expression of IFNGR, thus inhibiting the proliferation and promoting the apoptosis of GC cells. The results were consistent with the animal experiments on tumor-bearing gastric cancer mice. Conclusion: BXXX inhibited the expression of PD-L1 through multi-target and multi-pathway regulation of major oncogenes in GC, thus effect cell proliferation and apoptosis.

A case report of a post-polypectomy syndrome with severe sepsis and organ dysfunction Zhuang-Feng Zhuang, Zhen-Hao Ye, Zi-Shao Zhong, Gui-Hua He, Jing Wang, Sui-Ping Huang

Background: In the past, there were not a lot of studies on how A-kinase anchor protein 5 (AKAP5) involving in the pathogenesis and prognosis of non-mucin producing stomach adenocarcinoma (NMSA). Therefore, we studied the relationship between AKAP5 and the prognosis of NMSA and its possible mechanisms using publicly available data from The Cancer Genome Atlas (TCGA) Methods: RNA high-throughput sequencing and clinicopathologic data of NMSA were downloaded from the TCGA. Clinical pathologic features associated with AKAP5 expression were analyzed using the chi-square and Fisher exact tests. The relationship between the overall survival (OS) and AKAP5 expression was analyzed by the Kaplan-Meier method and the Cox regression analysis. GSEA analysis was performed using the TCGA dataset. Results: Our results indicated that the AKAP5 expression was increased in NMSA (all tumor vs. adjacent mucosa). Also, histologic grade, clinical stage, N classification, and survival status were significantly correlated with AKAP5 expression. Kaplan-Meier curves showed that low AKAP5 expression was associated with a poor OS among the NMSA patients (P=5.003e-05), and in the clinical stage III and IV (P=4.646e-05), TNM stage T3 (P=0.016), T4 (P=0.001), N2 (P=0.012), N3 (P=0.003), M0 (P=3.911e-05), and histological grade G3 (P=1.658e-04) subgroups. Cox regression analysis showed that reduced AKAP5 expression in NMSA is associated with age (HR =1.03, P=0.007), stage (HR =1.84 for stage I, II vs. stage III, IV, P=0.002) and M classification (HR =1.8 for M0 vs. M1, P=0.010). Gene sets related to cholesterol homeostasis, glycolysis, estrogen response late, adipogenesis, estrogen response early, notch signaling, and peroxisome were differentially enriched with the low AKAP5 expression phenotype. Conclusions: Low expression of AKAP5 may be a potential molecular marker for predicting poor prognosis of NMSA. Besides, cholesterol homeostasis, glycolysis, estrogen response, adipogenesis, notch signaling, and peroxisome may be the key pathways regulated by AKAP5 in NMSA. It also suggested that AKAP5 might potentially have biological functions in the development of stomach adenocarcinoma.