Aruchamy Mohanprasanth

Background: Streptococcus mutans (S. mutans) plays a major role in dental biofilm-related infections and contributes to antimicrobial resistance. Therefore, the development of biocompatible nanomaterials with antibacterial, antibiofilm, and regenerative properties is important for dental applications. Methods: In this study, hyaluronic acid and clove extract were used as natural precursors to synthesize hyaluronic acid-clove carbon dots (HCCDs) through a hydrothermal method. The synthesized HCCDs were characterized by XRD, FTIR, TEM, SEM, SAED and EDAX analysis. The antibacterial and antibiofilm activities against S. mutans were tested. Cell viability tests, AO/PI staining, morphological observation and wound-healing assays were used to evaluate cytocompatibility in MG-63 cells. Results: A broad peak (23.449) observed from XRD coincided with an amorphous graphitic carbon structure. TEM images showed the presence of a spherical nanostructure with an average size of 4 ± 2 nm. The FTIR result verified the presence of hydroxyl, carbonyl and oxygen-containing functional groups on the HCCD surface. Their synthesized HCCDs exhibited noteworthy antibacterial and antibiofilm activity with an MIC of 62.5 µg/mL against the S. mutans. Low toxicity toward MG-63 cells was observed, with 86% cell viability at 200 µg/mL in the cytocompatibility study. Additional good cellular compatibility was confirmed using AO/PI staining and morphological analysis. Furthermore, normal cell migration was observed, as wound healing assays showed no significant difference in closure between the treated and control groups. Conclusion: HCCDs exhibited antibacterial, antibiofilm, biocompatible, and wound-healing properties, highlighting their potential for dental nanomedicine and the treatment of oral biofilm-associated infections.

Background: The oral squamous cell carcinoma (OSCC) is a very aggressive cancer that is the product of tumor cell interactions with the microenvironment. The tumor microenvironment (TME) has a severe impact on OSCC progression, metastasis, and resistance to treatment by altering gene expression via various cellular and molecular signal transductions. Aim: This review systematizes the information on gene regulation in the OSCC TME (cellular components, signaling pathways that regulate tumor progression and resistance). Methods: We used PRISMA guidelines to search PubMed, Scopus, Web of Science, and Google Scholar (up to April 2025) with OSCC studies addressing the subject of gene regulation and tumor microenvironment. The quality of human or experimental models was evaluated using the Newcastle–Ottawa Scale and the qualitative synthesis was performed because of heterogeneity. Results: The significant regulatory functions of tumor-associated macrophages, cancer-associated fibroblasts, immune cells, and non-coding RNAs were found, especially in the pathways like JAK/STAT, EGFR, Wnt/ -β catenin, and PI3K/AKT/mTOR. Conclusions: The conceptualization of gene regulatory networks in the OSCC TME identifies the emerging biomarkers and targets of therapy. Merging multimodal omics and single-cell studies can further contribute to the precision strategies to enhance the outcomes of OSCC.

Trigonelline, a naturally derived bioactive compound, has gained interest for its potential anticancer properties. This study investigates its therapeutic efficacy against A549 lung cancer cells and elucidates the underlying molecular mechanisms. Cytotoxic effects were evaluated using MTT and Trypan blue exclusion assays in A549 cancer cells and biocompatibility were examined in 3T3-L1 mouse fibroblast cells. Flow cytometry was employed to analyze cell cycle distribution, apoptotic induction, and metabolic alterations were utilised using specific metabolic assay kits. Network analysis through the STRING database was performed to identify key signaling pathways affected by trigonelline. Gene expression changes were validated using RT-PCR, while Western blotting assessed protein levels of STAT2, BCL2, and BAX. Docking studies using AutoDock examined the binding affinity of trigonelline with STAT2-related targets, and molecular dynamics simulations evaluated the stability of trigonelline-bound STAT2 and BCL2 complexes using GROMACS package. Trigonelline exhibited significant cytotoxicity in A549 cells while showing minimal cell inhibitory effects in 3T3-L1 cells, indicating selective anticancer activity. Flow cytometry revealed that trigonelline induced G0/G1 cell cycle arrest and promoted apoptosis. Network and pathway analyses highlighted STAT2-mediated signaling, apoptosis, and metabolic regulation as major pathways influenced by trigonelline. RT-PCR results showed downregulation of genes involved in glycolysis and apoptosis. Western blot analysis confirmed decreased expression of STAT2 and the anti-apoptotic protein BCL2, alongside increased BAX protein levels. Docking studies demonstrated strong interactions with STAT2-associated targets, and molecular dynamics simulations confirmed the stable binding of trigonelline to STAT2 and BCL2. Trigonelline effectively inhibits the proliferation of A549 lung cancer cells by inducing cell cycle arrest, triggering apoptosis, modulating metabolic, and STAT2-mediated pathways. These findings suggest that trigonelline holds promise as a potential therapeutic candidate for lung cancer. Further in vivo studies and clinical investigations are warranted to explore its therapeutic potential.

Background/Objectives: The transformation of multifunctioning nanomaterials, incorporating antimicrobial activity and regenerative incompatibility, is becoming even more significant in the modern dental therapeutic context. Streptococcus mutans (S. mutans) is primarily linked to dental caries and pulp inflammation and requires new strategies that would be efficient at controlling the infection and promoting tissue repair. The objectives of the present research were to synthesize and critique the use of chitosan–eugenol carbon dots (CECDs) as a versatile nanoplatform in the field of dentistry to implement antimicrobial and regenerative dentistry. Methods: CECDs synthesized from biocompatible chitosan and eugenol were characterized by Scanning Electron Microscopy (SEM) and Energy Dispersive X-ray (EDX), evaluated from S. mutans inhibition via MIC/MBC, and assessed from cytocompatibility using 3T3-L1 fibroblast viability, morphology, and migration assays. Results: The resultant CECDs had a spherical morphology and a size of 5 ± 2 nm. The EDX analysis established the existence of carbon, nitrogen and oxygen labeling successful incorporation of heteroatoms, as well as surface functionalization. CECDs exhibited greater antibacterial effects against S. mutans through a concentration-dependent approach with MIC and MBC of 125 and 250 µg/mL respectively. Cytotoxicity assays indicated that the cells were viable, their morphology was intact, and that the cells moved more vigorously, which confirmed excellent biocompatibility. Conclusions: The synergistic combination of chitosan and eugenol into the carbon dot structure produced CECDs that had strong biomarker along with antibacterial activity and desirable cytocompatibility. These results indicate that CECDs are an attractive multifunctional nanoplatform in the treatment of oral infections and help with wound healing.

This review examines engineered combination nanomedicine strategies that integrate co-delivery platforms, tumor microenvironment targeting, and predictive translational models to overcome cancer drug resistance.

Chronic wounds remain a persistent clinical challenge due to their complex pathology involving prolonged inflammation, microbial biofilms, and impaired tissue regeneration. Emerging research highlights the dynamic role of the human microbiome in modulating immune responses and influencing wound healing outcomes. Disruptions to this microbial balance, termed dysbiosis, not only exacerbate infection but also hinder therapeutic efficacy. Recent advances in smart and sustainable nanotechnology offer promising avenues to address these challenges. By integrating microbiome-sensitive mechanisms with targeted delivery systems, bio-based nanomaterials can overcome multidrug resistance, modulate inflammation, and accelerate healing. This review explores the molecular interplay between chronic infections and host immunity, highlights next-generation nanomaterials for regenerative applications, and proposes a sustainable paradigm that bridges clinical effectiveness with environmental responsibility.