Carmen Marino is a Ph.D student at the University of Salerno. She gratuated in Science Biologists at the University of Sannio and specialized with honors in Biology at University of Salerno. From January to October 2020 carried out research, at the laboratory of Pharmaceutical Chemistry of Professor Anna Maria D'Ursi, within the project called "Fighting cancer resistance: integrated multidisciplinary platform for a project innovative technology to oncotherapies". Currently enrolled in the third year of PhD in Pharmaceutical Sciences, she dedicates herself to Research "Metabolomics approach in the study of molecular mechanisms of pathologies and in identification of new pharmacological targets".
EDUCATION
She graduated in Science Biologists at the University of Sannio and specialized with honors in Biology at University of Salerno. From January to October 2020 carried out research, at the laboratory of Pharmaceutical Chemistry of Professor Anna Maria D'Ursi, within the project called "Fighting cancer resistance: integrated multidisciplinary platform for a project innovative technology to oncotherapies". She holds a PhD in pharmaceutical sciences and is currently a research fellow at UNISA
RESEARCH INTERESTS
Carmen has focused her studies on biology field, in particular in omics techniques. Since her thesis period she has focused on the characterization of metabolomic profiles obtained through the analysis of biofluids and tissues with NMR spectroscopy.
Analyzing Nicotine Action Against Amyloid Toxicity by NMR-Pharmacometabolomics: An Exploratory Study Enza Napolitano, Carmen Marino, Manuela Grimaldi, Michela Buonocore, Angelo Santoro, et al. NMR in Biomedicine, 2026 Alzheimer's disease ( AD ) is the primary neurodegenerative disease spread worldwide. One of the main histopathological hallmarks of AD is the deposition of amyloid plaques in the brain. Despite some epidemiological studies demonstrating that cigarette smoke is a factor in predisposing people to AD , nicotine, the principal alkaloid of Nicotiana Tobacco , has been widely studied for its ability to improve cognitive performance, both in animal models and in human studies. Several hypotheses have been proposed to explain the mechanism of action underlying the beneficial effect of nicotine in AD ; however, this is still questioned. To gain new insights into the molecular mechanism underlying nicotine's neuroprotective action in AD , we performed NMR metabolomics on SH‐SY5Y neuroblastoma cells treated with Aβ(1–42) in the presence of nicotine. Our data show that the neuroprotective action of nicotine resides in its ability to restore the systemic unbalanced metabolism associated with AD . In particular, nicotine reverses most Aβ(1–42)‐induced metabolic impairments, including those related to amino acid metabolism, especially neurotransmission, as well as alterations in energy and membrane phospholipid metabolism.
Cell Surface Markers of Mesenchymal Stem Cells: Current Knowledge and Advances in Characterization Technologies Angelo Santoro, Manuela Grimaldi, Carmen Marino, Enza Napolitano, Michela Buonocore, et al. Life, 2026 Mesenchymal stem cells (MSCs) are pivotal in regenerative medicine due to their high differentiation potential and therapeutic versatility. MSCs are multipotent cells capable of differentiating into adipocytes, chondroblasts, osteoblasts, and, under specific conditions, neural, myocyte, and epidermal lineages. This cell type contributes to tissue repair, immunomodulation, and regenerative therapies for cardiac, orthopedic, and hematological disorders. Accurate identification and characterization of these stem cells are essential for both research and clinical applications. MSCs are typically defined by plastic adherence, expression of surface markers CD105, CD73, and CD90, low or absent expression of hematopoietic markers (CD45, CD34), and in vitro differentiation potential. Understanding the expression patterns and functional relevance of these surface markers is critical for improving isolation strategies, enhancing therapeutic efficacy, and minimizing adverse effects. This review provides a comprehensive overview of the principal surface markers of MSCs, highlighting their significance in stem cell biology and clinical translation.
Effects of Nicotine on SH-SY5Y Cells: An NMR-Based Metabolomic Study Enza Napolitano, Carmen Marino, Manuela Grimaldi, Michela Buonocore, Anna Maria D’Ursi Metabolites, 2025 Background/Objectives: Nicotine is a naturally occurring alkaloid primarily found in Nicotiana tabacum. This phytochemical is well known for its addictive properties, and its consumption—particularly through tobacco smoking—is strongly associated with an increased risk of malignancies, metabolic dysfunctions, and cardiovascular as well as respiratory diseases. Despite these adverse effects, several studies have also reported beneficial actions of nicotine, including the enhancement of cognitive functions in several neurodegenerative diseases. Methods: To better elucidate the multiple effects of nicotine and clarify their underlying mechanisms, we performed an NMR-based metabolomic analysis of SH-SY5Y neuroblastoma cells exposed to nicotine action. Results: Our results indicate that nicotine modulates mitochondrial function and membrane turnover, thereby influencing mitochondrial bioenergetics, synaptic plasticity, and connectivity. Conclusions: Collectively, these findings may contribute, at least in part, to explaining the neuroprotective effects of nicotine described in preclinical models of neurodegenerative disease.
Modulation of Gut Bacterial and Fungal Microbiota in Fibromyalgia Patients Following a Carb-Free Oloproteic Diet: Evidence for Candida Suppression and Symptom Improvement Giuseppe Castaldo, Maria D’Elia, Mariagrazia De Prisco, Veronica Folliero, Carmen Marino, et al. Microorganisms, 2025 Fibromyalgia (FM) is a complex chronic syndrome characterized by widespread pain, fatigue, and gastrointestinal complaints. Clinical observations and preliminary metabolomic data suggest a possible link between symptom severity and intestinal dysbiosis, including fungal overgrowth. This study investigates whether a carb-free oloproteic diet can beneficially modulate the gut microbiota in FM patients. Thirty-four female patients with diagnosed FM were enrolled in a controlled, parallel-arm nutritional intervention. Group FM1 (n = 22) followed a 45-day carb-free oloproteic diet followed by a 45-day low-glycemic (LOGI) diet. Group FM2 (n = 12) received a continuous LOGI diet for 90 days. They were collected at baseline (T0), after 45 days (T45), and at 90 days (T90). Microbial profiles were analyzed by 16S and 18S rRNA gene sequencing to assess bacterial and fungal composition. In FM1, the oloproteic phase led to a marked reduction in fungal abundance (Ascomycota) and an increase in butyrate-producing bacteria such as Faecalibacterium and Roseburia. These changes were partially reversed after the LOGI phase. In FM2, no significant microbiota shifts were observed. Clinical improvements paralleled microbiota modulation only in FM1. The carb-free oloproteic diet may support gut microbial rebalancing in FM, particularly through transient suppression of fungal overgrowth. These findings support further investigation into nutritional strategies targeting dysbiosis in FM management.
Impact of a Formulation Containing Chaga Extract, Coenzyme Q10, and Alpha-Lipoic Acid on Mitochondrial Dysfunction and Oxidative Stress: NMR Metabolomic Insights into Cellular Energy Maria D’Elia, Carmen Marino, Rita Celano, Enza Napolitano, Chiara Colarusso, et al. Antioxidants, 2025 Objectives: The aim of this study was to evaluate the impact of a novel antioxidant formulation (RE:PAIR, RP-25) containing CoQ10, alpha-lipoic acid, and Chaga extract on mitochondrial dysfunction and oxidative stress. To explore the activity of the formulation on neuronal cells, we explored cell metabolism and its activity as an antioxidant, using a combination of NMR-based metabolomics and UHPLC-HRMS analytical techniques. Methods: SH-SY5Y neuroblastoma cells were treated with RP-25, and cell viability was assessed via CCK-8 assay. Metabolomic profiles of the treated and untreated cells were analyzed by 1D-NMR, providing insights into both intracellular metabolites (endometabolome) and excreted metabolites (exometabolome). Additionally, a UHPLC-HRMS method was developed for quality control and analysis of the RP-25 formulation. Multivariate statistical approaches, including PLS-DA and volcano plot analyses, were used to identify key metabolic changes. Changes in mitochondrial membrane potential were assessed by means of TMRE assay, while radical oxygen species (ROS) were measured by means of the DCHF assay. Results: RP-25 treatment did not affect cell viability but significantly increased metabolic pathways, including amino acid biosynthesis, oxidative phosphorylation, and glycolysis. Higher levels of ATP, glutamate, tyrosine, and proline were observed in treated cells than in control cells, indicating enhanced cellular energy production, as also proved by the increased stability of the mitochondrial membrane after RP-25 treatment, an index of preserved mitochondrial functions. In support, the formulation RP-25 showed antioxidant activity when cells underwent peroxide oxygen stimulation. This effect was mainly due to the combination of Chaga, CoQ10, and ALA, main components of the RP25 formulation. Moreover, the analysis of enriched pathways highlighted that RP formulation influenced mitochondrial energy and oxidative stress response. Conclusions: RP-25 demonstrated biological activity in that it mitigated mitochondrial dysfunction and oxidative stress in neuronal cells, with potential implications in neuronal diseases associated with dysfunctional mitochondria.
