Vol 27, No 13 (2024)

Alzheimer’s disease is one of the neurodegenerative diseases which causes cognition deficit. There are currently few medications available to treat Alzheimer's disease, even though researchers have devoted a great deal of time studying the condition and offering many benefits. Thus, only a few drugs are available for the treatment of Alzheimer’s disease. Amentoflavone is a dietary component found in many plants and herbs that has several health advantages. Amentoflavone has demonstrated strong protective benefits against a range of brain illnesses in preclinical trials, most frequently in Alzheimer's disease. Amentoflavone, a biflavonoid, can be identified in a variety of herbs upon isolation. Considering the beneficial properties of this compound, this review emphasizes the pharmacological effects and botanical sources of amentoflavone, as well as the compound's benefits and possible applications in the treatment of Alzheimer's disorders.

Introduction:When the body experiences a change in its internal environment due to factors such as mood (euphoria, stress) and illness, it releases biomarkers in large quantities. These biomarkers are used for detecting a disease at its early stages. This involves the detection of insufficient quantities of biocomponents, which can be done by using nanomaterials, conventional materials, and biotechnology; thus, scientists can increase the sensitivity of electrochemical sensors. According to studies conducted in this area, electrochemical sensors have shown promise as a diagnostic tool due to their ability to identify and pinpoint illness biomarkers. The present review article was compiled to gather the latest information on electrochemical biosensors targeting stress markers.

Materials and Methods:The authors searched scholarly databases like ScienceDirect, Pubmed, Medline, and Scopus for information on electrochemical biosensors targeting stress markers.

Results:In this article, we looked at the recent developments in electrochemical sensors for stress monitoring. Because of advances in nanomaterial and biomolecule processes, electrochemical biosensors have been developed with the sensitivity to detect several biomarkers in real-time in therapeutically relevant materials.

Conclusion:This biomarker sensor strategy can analyze various biofluids (sweat, plasma, urine, and saliva).

Objective:This study aimed to explore the key alternative splicing events in costimulatory molecule-related genes in colon cancer and to determine their correlation with prognosis.

Methods:Gene expression RNA-sequencing data, clinical data, and SpliceSeq data of colon cancer were obtained from The Cancer Genome Atlas. Differentially expressed alternative splicing events in genes were identified, Followed by correlation analysis of genes corresponding to differentially expressed alternative splicing events with costimulatory molecule-related genes. Survival analysis was conducted using differentially expressed alternative splicing events in these genes and a prognostic model was constructed. Functional enrichment, proteinprotein interaction network, and splicing factor analyses were performed.

Results:In total, 6504 differentially expressed alternative splicing events in 3949 genes were identified between tumor and normal tissues. Correlation analysis revealed 3499 differentially expressed alternative splicing events in 2168 costimulatory molecule-related genes. Moreover, 328 differentially expressed alternative splicing events in 288 costimulatory molecule-related genes were associated with overall survival. The prognostic models constructed using these showed considerable power in predicting survival. The ubiquitin A-52 residue ribosomal protein fusion product 1 and ribosomal protein S9 were the hub nodes in the protein-protein interaction network. Furthermore, one splicing factor, splicing factor proline and glutamine-rich, was significantly associated with patient prognosis. Four splicing factor-alternative splicing pairs were obtained from four alternative splicing events in three genes: TBC1 domain family member 8 B, complement factor H, and mitochondrial fission 1.

Conclusion:The identified differentially expressed alternative splicing events of costimulatory molecule-related genes may be used to predict patient prognosis and immunotherapy responses in colon cancer.

aims:To explore the potential roles and mechanisms of shikonin in gastric cancer by network pharmacology and biological experiments.

background:Gastric cancer is one of the most common and deadly cancers in the world. Although the survival rate of gastric cancer has improved worldwide for many years, it is difficult to treat due to its high tumor recurrence and easy resistance to chemotherapeutic drugs.Recently studies showed that traditional Chinese medicine Shikonin had anti-cancer effects with their unique advantages of high efficiency and small side effect.

objective:To study the potential roles and mechanisms of shikonin in gastric cancer by network pharmacology and biological experiments.

method:The key genes and targets of shikonin in gastric cancer were predicted by network pharmacology and molecular docking study. The effect of shikonin on the proliferation, migration and invasion of gastric cancer cells was detected by the CCK8 method, Wound healing and Transwell assays. The expression levels of c-Myc and Yap-1 protein in gastric cancer cells after shikonin intervention were detected by western blotting.

result:The study of network pharmacology found that the key target genes of shikonin on gastric cancer cells were c-Myc, Yap-1, AKT1,etc. GO and KEGG analysis showed regulation of cell migration, proliferation, adhesion and other biological processes; PI3K-Akt signaling pathway, HIF-1 signaling pathway, necroptosis and other cancer pathways. Molecular docking showed that shikonin was most closely combined with protooncogene c-Myc and Yap-1. In vitro experiments showed that the proliferation rate, migration and invasion ability of gastric cancer cell group decreased significantly after shikonin intervention for 24h, and it was concentration-dependent. The expression levels of c-Myc and Yap-1 in gastric cancer cells were significantly decreased after shikonin intervention.

conclusion:This study showed that protooncogene c-Myc and Yap-1 were the core target genes of shikonin on gastric cancer cells. Shikonin may suppress gastric cancer cells by inhibiting the protooncogene c-Myc and Yap-1. It suggested shikonin maybe a good candidate for the treatment of gastric cancer.

Background::Interstitial cystitis is a diagnosis of exclusion due to the complexity of its etiology and pathology, which is a chronic disease with an unknown etiology. To our knowledge, few studies were performed to identify predictive biomarkers for interstitial cystitis.

Objective::This study aimed to identify and validate potential biomarkers for interstitial cystitis (IC).

Methods::The interstitial cystitis datasets were retrieved from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified by using the R package and were subjected to functional and pathway enrichment analysis. Key biomarkers of interstitial cystitis were identified by using Lasso regression analysis and the SVM-RFE algorithm. The diagnostic value of key biomarkers was validated in internal and external datasets, and pathways that relate to biomarkers of interstitial cystitis were screened. The ssGSEA was employed to identify the immune cells closely related to biomarkers. The expression of PLAC8 in patients with interstitial cystitis was detected by immune-histochemistry (IHC).

Results::Sixteen differentially expressed genes associated with interstitial cystitis were identified, which were primarily linked to the biological process of the chemokine signaling pathway. PLAC8, identified as a biomarker for interstitial cystitis, was validated to express a significantly different between IC and normal bladder tissues. PLAC8-related pathways were analyzed, with a focus on NF-κB, TNF, Toll-like receptor, chemokine, IL-17, and JAK-STAT signaling pathways. PLAC8 was proved to be closely related to immune activations, which is similar to the pathogenesis of IC, which is a chronic dysregulated immune disease. Meanwhile, we also observed a higher level of PLAC8 in IC tissues.

Conclusion::PLAC8 has promising application prospects as a biomarker for interstitial cystitis diagnosis. These findings could aid in the diagnosis and treatment of interstitial cystitis.

Background:Lung adenocarcinoma (LUAD) is one of the most common malignant cancers. Neutrophil extracellular traps (NETs) have been discovered to play a crucial role in the pathogenesis of LUAD. We aimed to establish an innovative prognostic model for LUAD based on the distinct expression patterns of NETs-related genes.

Methods:The TCGA LUAD dataset was utilized as the training set, while GSE31210, GSE37745, and GSE50081 were undertaken as the verification sets. The patients were grouped into clusters based on the expression signature of NETs-related genes. Differentially expressed genes between clusters were identified through the utilization of the random forest and LASSO algorithms. The NETs score model for LUAD prognosis was developed by multiplying the expression levels of specific genes with their corresponding LASSO coefficients and then summing them. The validity of the model was confirmed by analysis of the survival curves and ROC curves. Additionally, immune infiltration, GSEA, mutation analysis, and drug analysis were conducted. Silencing ABCC2 in A549 cells was achieved to investigate its effect.

Results:We identified six novel NETs-related genes, namely UPK1B, SFTA3, GGTLC1, SCGB3A1, ABCC2, and NTS, and developed a NETs score signature, which exhibited a significant correlation with the clinicopathological and immune traits of the LUAD patients. High-risk patients showed inhibition of immune-related processes. Mutation patterns exhibited variability among the different groups. AZD3759, lapatinib, and dasatinib have been identified as potential candidates for LUAD treatment. Moreover, the downregulation of ABCC2 resulted in the induction of apoptosis and suppression of migration and invasion in A549 cells.

Conclusion:Altogether, this study has identified a novel NET-score signature based on six novel NET-related genes to predict the prognosis of LUAD and ABCC2 and has also explored a new method for personalized chemo-/immuno-therapy of LUAD.

Background::The co-morbidity of DMOB has become increasingly problematic among the world's population because of a high-calorie diet and sedentary lifestyle. DMOB is associated with lower testosterone (TN) levels, the male sex hormone. The phytochemical compound silymarin (SN) exerts antidiabetic activity by modifying β-cells and anti-obesity activity by inhibiting adipogenesis by methylxanthine.

Aim::The goal of this study was to find out how well testosterone (TN) with silymarin (SN) protects against oxidative stress and inflammation in the liver of the experimental rats with type 2 diabetes (T2D) and obesity (DMOB).

Objectives::The present study evaluates the efficacy of TN and SN combination (TNSN) on the levels of the potential parameters, such as body mass, serum marker enzymes, fasting glucose levels, HbA1c levels, lipid profile, enzymatic and non-enzymatic antioxidants, proinflammatory cytokines, gene expression pathways, and histopathology in a DMOB comorbidity rat model.

Methods::Male Sprague-Dawley (SD) rats were fed a high-fat diet (HFD) for 20 weeks with an administration of a single dose of streptozotocin (STZ) i.p. injection (30 mg/kg) on the 9th week of the study. The procedure was to develop the DMOB co-morbidity model in the experimental animals. Co-treatment of TN and SN administration were followed throughout the experiment. Rats were sacrificed after overnight fasting to collect serum and liver tissue samples. Samples were analyzed using a clinical chemistry automated analyzer, spectrophotometry, and quantitative real-time PCR (qPCR) methods and protocols.

Results::Analyses of body mass changes, serum marker enzymes, fasting glucose levels, HbA1c levels, lipid profiles, enzymatic and non-enzymatic antioxidants, TNF-α, IL-6, adiponectin, CYP7A1, ACC expression pathways, and histopathology showed significant abnormal levels (P ≤ 0.05) in the pathological group. These were efficiently treated to normal by the administration of TNSN.

Conclusion::These results concluded that TNSN exerted protective efficacy against the liver abnormalities in the co-morbidity of the DMOB rat model.