Rosanna Avola

Contemporary research in food chemistry, pharmacognosy, and translational sciences is undergoing a profound methodological convergence

The investigation of natural bioactive compounds represents a cornerstone of contemporary scientific research, with profound implications for clinical medicine, nutraceuticals, cosmetics, and biotechnology

The genus Oenanthe L. (Apiaceae) comprises aquatic and semi-aquatic species widely distributed across the Northern Hemisphere, some of which are traditionally used as food or in folk medicine. Despite this ethnobotanical relevance and toxicological notoriety, phytochemical and pharmacological data on the genus remain limited, especially regarding their essential oils (EOs). Essential oils, extracted by hydrodistillation from aerial parts of Sicilian Oenanthe fistulosa L. (OF), Oenanthe aquatica (L.) Poir (OA), and Oenanthe pimpinelloides L. (OP), were analyzed by GC–MS. The EO of O. fistulosa was dominated by monoterpene hydrocarbons (59.8%), with β-cis-ocimene (21.6%), sabinene (9.3%), and β-trans-ocimene (8.4%) as the main metabolites. O. pimpinelloides also exhibited a monoterpene-rich profile (60.3%), characterized by β-cis-ocimene (15.5%), sylvestrene (12.8%), and β-trans-ocimene (10.3%) but distinguished by a high apiol content (21.0%), indicating a mixed monoterpene/phenylpropanoid chemotype. In contrast, O. aquatica revealed a markedly different profile dominated by phenylpropanoids (57.2%), particularly dill apiol (53.5%), alongside α-pinene (17.2%) and sabinene (6.5%), representing an uncommon chemotype within the genus. This study aimed to evaluate whether these chemo-diverse Sicilian Oenanthe EOs (dill-apio OA 53.5%; ocimene OF 59.9%; apiol OP 21%) differentially modulated LPS-induced epithelial redox stress in Caco-2. Caco-2 cells were treated for 24 h with lipopolysaccharide (LPS) and co-treated with two concentrations (12.5 and 25 µg/mL) of EOs from three different species of Oenanthe. Assessment of proliferating cell nuclear antigen (PCNA) and the stress response of enzyme heme oxygenase-1 (HO-1) expression was performed using Western blot and reverse transcriptase-polymerase chain reaction (RT-PCR). EOs showed species- and concentration-dependent effects on LPS-induced stress in Caco-2 cells. O. aquatica and O. fistulosa EOs exerted cytoprotective and antioxidant activity at low concentrations (12.5 and 25 μg/mL), reducing 8-hydroxy-2′ -deoxyguanosine (8-OHdG) DNA damage and moderately upregulating HO-1. In contrast, O. pimpinelloides EO (apiol-rich) induced dose-dependent cytotoxicity, elevated 8-OHdG despite strong HO-1 induction, and lacked protection at higher doses. PCNA expression was reduced by LPS across all treatments, with no preservation of proliferation by any EOs. These findings reveal chemotype-specific modulation of oxidative stress and epithelial integrity.

Background/Objectives: Rare diseases are a wide and heterogeneous group of multisystem life-threatening or chronically debilitating clinical conditions with reduced life expectancy and a relevant mortality rate in childhood. Some of these disorders have typical neurological symptoms, presenting from birth to adulthood. Dietary patterns and nutritional compounds play key roles in the onset and progression of neurological disorders, and the impact of alimentary needs must be enlightened especially in rare neurological diseases. This work aims to collect the in vitro, in vivo, and clinical evidence on the effects of diet and of nutrient intake on some rare neurological disorders, including some genetic diseases, and rare brain tumors. Herein, those aspects are critically linked to the genetic, biological, biochemical, and pathophysiological hallmarks typical of each disorder. Methods: By searching the major web-based databases (PubMed, Web of Science Core Collection, DynaMed, and Clinicaltrials.gov), we try to sum up and improve our understanding of the emerging role of nutrition as both first-line therapy and risk factors in rare neurological diseases. Results: In line with the increasing number of consensus opinions suggesting that nutrients should receive the same attention as pharmacological treatments, the results of this work pointed out that a standard dietary recommendation in a specific rare disease is often limited by the heterogeneity of occurrent genetic mutations and by the variability of pathophysiological manifestation. Conclusions: In conclusion, we hope that the knowledge gaps identified here may inspire further research for a better evaluation of molecular mechanisms and long-term effects.

Neuroinflammation, a pivotal factor in the pathogenesis of various brain disorders, including neurodegenerative diseases, has become a focal point for therapeutic exploration. This review highlights neuroinflammatory mechanisms that hallmark neurodegenerative diseases and the potential benefits of essential oils in counteracting neuroinflammation and oxidative stress, thereby offering a novel strategy for managing and mitigating the impact of various brain disorders. Essential oils, derived from aromatic plants, have emerged as versatile compounds with a myriad of health benefits. Essential oils exhibit robust antioxidant activity, serving as scavengers of free radicals and contributing to cellular defense against oxidative stress. Furthermore, essential oils showcase anti-inflammatory properties, modulating immune responses and mitigating inflammatory processes implicated in various chronic diseases. The intricate mechanisms by which essential oils and phytomolecules exert their anti-inflammatory and antioxidant effects were explored, shedding light on their multifaceted properties. Notably, we discussed their ability to modulate diverse pathways crucial in maintaining oxidative homeostasis and suppressing inflammatory responses, and their capacity to rescue cognitive deficits observed in preclinical models of neurotoxicity and neurodegenerative diseases.

Wilms’ tumor gene 1 silencing inhibits proliferation of human osteosarcoma MG-63 cell line by cell cycle arrest and apoptosis activation Wilms’ tumor gene 1 silencing inhibits proliferation of human osteosarcoma MG-63 cell line by cell cycle arrest and apoptosis activation

Krabbe disease is a genetic demyelinating syndrome characterized by deficiency of the enzyme β-galactosylceramidase, lysosomal psychosine accumulation, and loss of myelin-forming cells. In this study, some apoptotic markers such as apoptotic index (AI), DNA fragmentation, caspase-3, PTEN, Bad, and PI3K were determined in oligodendrocyte precursors from wild type or twitcher mice untreated or treated with psychosine. Twitcher is a natural mouse model of Krabbe disease containing a premature stop codon (W339X) in the β-galactosylceramidase gene. Moreover, a possible involvement of connexin (Cx)43 in cell death of oligodendrocyte precursors induced by psychosine was investigated with the final aim to provide a contribution to the knowledge of the molecular mechanisms and pathophysiological events that occur in Krabbe disease. Connexins are a multigene family of structurally related trans-membrane proteins able to modulate essential cellular processes such as proliferation, differentiation and migration. Among these, Cx43 is the predominant isoform in many cell types, including neural progenitor cells. Our results showed an increase of AI, DNA fragmentation, caspase-3, PTEN, Bad, and Cx43 associated to a decrease of PI3K, pAKT and pBad. Taken together, these findings suggest an involvement of Cx43 in the psychosine-mediated apoptosis of primary oligodendrocyte progenitors from wild type or twitcher mice, used for the first time as cell models in comparison. It could open unexplored perspective also for other demyelinating diseases.