Current Pharmaceutical Biotechnology - Volume 27, Issue 1, 2026

Dilated Cardiomyopathy (DCM) is a debilitating cardiovascular disorder that challenges current therapeutic strategies. The exploration of novel drug repositioning opportunities through gene expression analysis offers a promising avenue for discovering effective treatments.

This study aims to identify potential drug repositioning opportunities and lead compounds for DCM treatment by optimizing gene expression characteristics using published data.

Our approach involved analyzing DCM expression profiles from the Gene Expression Omnibus database and identifying differentially expressed genes with GEO2R. A protein interaction network was constructed using the STRING database and visualized with Cytoscape. Enrichment analyses were conducted on these genes through the Omicshare platform, followed by the identification of candidate compounds via the Connectivity Map (CMAP) and validation through molecular docking. The Coremine Medical database was utilized to predict potential herbal medicines.

We identified 29 differentially expressed genes, highlighting MYH6, NPPA, and NPPB as central to DCM pathology. Enrichment analyses indicated significant impacts on biological processes, such as organ morphogenesis and inflammatory responses. The AGE-RAGE signaling pathway was notably affected. From over 6,100 compounds analyzed, tenoxicam emerged as a promising candidate, with Radix Salviae Miltiorrhizae (Danshen) being suggested as a potential herbal treatment.

This study underscores the utility of bioinformatics in uncovering new therapeutic candidates for DCM, offering a foundational step towards novel drug development.

The objective of this study is to conduct network toxicology analysis based on smoking habits and develop a simpler and more effective toxicology product ingestion control system.

Smoking behavior can affect the pathogenesis and prognosis of neuroimmune gastrointestinal diseases.

The purpose of developing tools to assist clinical practice is to avoid the harm of cigarettes to the human body.

Molecular dynamics method was used to elucidate the biophysical mechanism of TP53 gene mutation caused by harmful ingredients, and the signaling pathway of midbrain edge excitation was determined by molecular dynamics of nicotine and dopamine receptor D3. The possible involvement of nicotine in neuronal damage was determined through the molecular interaction between nicotine and ACHE. Molecular pathways were analyzed based on the aforementioned biological principles, developed artificial intelligence systems and brain computer interface systems.

Several signaling pathways were elucidated, and effective AI algorithms were developed.

The accuracy of artificial intelligence systems is over 70%. This study provides clinical doctors with a new precision medicine strategy and tool to regulate patient behavior and reduce disease risk.

This project was approved by the Ethics Committee of Chifeng Cancer Hospital and reported to the WHO.

A stone is a compact mass of one or more crystallised substances. The essential mechanism of stone formation is an excessive concentration of poorly soluble compounds in the urine. In excessive concentration, these compounds precipitate into crystals, which then aggregate to form a stone. The use of certain plants using the turbidimetric model has shown positive results on oxalocalcic crystallisation and, according to a recent study, has revealed very high inhibition rates.

The aim of this study was to dissolve calcium oxalate urinary stones using two medicinal plants with high inhibition rates by monitoring Ca²⁺ release, pH variation, and mass loss. The study consisted of treating the stones with two plants, Ficus-carica and Zea mays, at two concentrations of 10g/l and 25g/l for 24 hours.

The main analytical techniques used in this study were as follows: Morphological analysis using a binocular magnifying glass, Fourier transform infrared spectroscopic method, and potentiometric method along with specific calcium electrode and an analytical balance. The study on the release of Ca²⁺ in the presence of the different herbal teas during 8 treatments of 3 to 4 hours was carried out on a series of 33 stones with the same chemical composition from several spontaneous expulsions of a 43-year-old male subject with lithiasis.

The results showed a very remarkable effect of the Ficus-carica plant on Ca²⁺ release, which recorded 156.98 ppm, while Zea mays gave 130.63 ppm.

The kinetics of Ca²⁺ release were monitored by a potentiometer using a Ca^2+-specific electrode. Zea mays at 10g/l showed a slightly positive effect on calculus dissolution compared to Ficus-carica.

Diabetic Kidney Disease (DKD) is a major cause of End-Stage Renal Disease (ESRD) and lacks effective treatments. Tangmaikang Granules (TMK), a multi-herb traditional Chinese medicine formulation, have shown potential in managing DKD. However, the precise active components, molecular mechanisms, and therapeutic advantages of TMK remain unclear.

This study tests the hypothesis that TMK granules exert protective effects on DKD by targeting multiple pathways involved in oxidative stress, inflammation, and apoptosis in podocytes through a multi-targeted approach. The aim was to identify TMK’s bioactive components, evaluate its therapeutic potential, and uncover its molecular mechanisms in DKD.

The bioactive constituents in TMK were determined through ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). Drug targets were identified using SwissTargetPrediction and SuperPred, whereas DKD-associated targets were obtained from the GeneCards, DisGeNET, OMIM, and TTD databases. A Protein-Protein Interaction (PPI) network was constructed, and key targets were identified via topological analysis. Molecular docking and dynamics simulations were performed to evaluate stable binding interactions. GO and KEGG pathway enrichment analyses were conducted to uncover relevant signaling pathways. TMK's effects on oxidative stress, inflammation, and apoptosis in podocytes were assessed using CCK-8, flow cytometry, RT-qPCR, ELISA, and Western blot assays.

Thirty active compounds and 384 potential therapeutic targets were identified, with eight key targets. Pathway enrichment analysis revealed TMK’s involvement in AGE-RAGE, EGFR, HIF-1, and apoptosis pathways, affecting inflammatory cytokine responses and oxidative stress. In vitro experiments demonstrated that TMK significantly reduced oxidative stress, inflammation, and apoptosis in podocytes by inhibiting the MAPK and NF-κB pathways.

TMK granules target DKD through a multi-component, multi-target strategy, effectively mitigating oxidative stress and suppressing inflammatory and apoptotic pathways. This study integrates advanced computational and experimental methods, demonstrating TMK’s unique therapeutic potential and providing a robust foundation for its clinical application in DKD management.

Traditional Chinese medicine has been widely used to treat gastric cancer, but the effect of the Weinaian capsule on gastric cancer is still unclear.

This study aimed to find the potential therapeutic targets and pharmacological mechanisms of Weinaian capsule in gastric cancer.

We employed the network pharmacological analysis to find the therapeutic targets. Firstly, we searched the bioactive components of Weinaian capsule in TCMSP and the Swiss database. We downloaded disease gastric cancer targets from the GeneCards database and used the Venn diagram to identify common targets for disease and drugs. Then, we performed GO and KEGG pathway enrichment analyses, used the Cytoscape software to screen core targets and components, and constructed a drug-disease-target network. In addition, visual molecular docking and molecular dynamics simulation of targets and components with strong affinity were performed. Finally, we verified the effect of the drug on cell proliferation and metastasis using CCK8, clonal formation, and wound healing assays, and investigated the molecular mechanism by qRT-PCR.

A total of 33 bioactive components were procured; 128 common targets for gastric cancer and drugs were screened. The GO and KEGG pathway enrichment analyses showed the PI3K-AKT pathway to be at the top. The core target AKT1 and the core component isorhamnetin exhibited the strongest molecular binding force and good binding stability. Compared to the control group, Weinaian capsule group inhibited gastric cancer cell proliferation and migration by down-regulating the expressions of PI3K and AKT.

Weinaian capsule inhibited cell proliferation and metastasis by affecting the PI3K-AKT pathway in gastric cancer.

Hydroxysafflor Yellow A (HSYA), known for its anti-inflammatory effects in cardiovascular diseases, has also been shown to reduce adiposity and improve metabolic disorders in diet-induced obese (DIO) mice. However, the molecular mechanisms underlying its anti-obesity effects, particularly whether they are mediated through immune-inflammatory pathways, remain unclear. This study aims to identify the key molecular mechanisms involved in HSYA's anti-obesity action.

Male C57BL/6J mice were divided into three groups: Standard Feed (SF), High-Fat Diet (HFD), and HFD with HSYA treatment (250 mg/kg/day for 9 weeks). Whole transcriptome sequencing of White Adipose Tissue (WAT) identified Differentially Expressed Genes (DEGs), which were integrated with network pharmacology predictions to identify key molecular targets of HSYA. RT-qPCR in WAT, 3T3-L1 adipocytes, and RAW264.7 macrophages validated the core genes, and molecular docking assessed HSYA’s binding affinity with these targets.

HSYA treatment significantly reduced body weight (35.27 ± 1.27g vs. 45.46 ± 1.68g, p < 0.05) and WAT mass (3.38±0.21g vs. 1.86±0.27g, p < 0.05) in DIO mice and ameliorated glucose and lipid metabolism abnormalities. Transcriptome analysis revealed 739 DEGs, with 21 overlapping genes identified between sequencing and network pharmacology analyses. Experimental validation highlighted Prkcd, Btk, and Vav1 as core genes within immune-inflammatory pathways, including chemokine and B cell receptor signaling, which are implicated in obesity-related inflammation. RT-qPCR confirmed the downregulation of Prkcd, Btk, and Vav1 after HSYA treatment, consistent with transcriptomic findings. Molecular docking analysis demonstrated strong binding affinities between HSYA and VAV1 (-8.5 kcal/mol), BTK (-6.9 kcal/mol), and PRKCD (-6.6 kcal/mol).

HSYA demonstrates the therapeutic potential for obesity by modulating immune-inflammatory pathways in WAT, specifically targeting Prkcd, Btk, and Vav1 in mice. Given its clinical use in cardiovascular disease, these findings suggest that HSYA may offer broader therapeutic benefits, including obesity management, though further studies are needed to clarify the mechanisms and assess its applicability to humans.