In December 2019, a novel coronavirus, COVID-19, was discovered to be the causal agent of a severe respiratory infection named SARS-CoV-2, and it has since been recognized worldwide as a pandemic. There are still numerous doubts concerning its pathogenesis and particularly the underlying causes of the various clinical courses, ranging from severe manifestations to asymptomatic forms, including acute respiratory distress syndrome. The major factor responsible for acute respiratory distress syndrome is the so-called “cytokine storm,” which is an aberrant response from the host immune system that induces an exaggerated release of proinflammatory cytokines/chemokines. In this review, we will discuss the role of cytokine storm in COVID-19 and potential treatments with which counteract this aberrant response, which may be valuable in the clinical translation.

Neurodegenerative disease etiology is still unclear, but different contributing factors, such as lifestyle and genetic factors are involved. Altered components of the gut could play a key role in the gut-brain axis, which is a bidirectional system between the central nervous system and the enteric nervous system. Variations in the composition of the gut microbiota and its function between healthy people and patients have been reported for a variety of human disorders comprising metabolic, autoimmune, cancer, and, notably, neurodegenerative disorders. Diet can alter the microbiota composition, affecting the gut-brain axis function. Different nutraceutical interventions have been devoted to normalizing gut microbiome dysbiosis and to improving biological outcomes in neurological conditions, including the use of probiotics. Preclinical and clinical investigations discussed in this review strengthen the correlation between intestinal microbiota and brain and the concept that modifying the microbiome composition may improve brain neurochemistry, modulating different pathways. This review will discuss the potential use of probiotics for Parkinson’s disease prevention or treatment or as adjuvant therapy, confirming that gut microbiota modulation influences different pro-survival pathways. Future investigations in Parkinson’s disease should consider the role of the gut-brain axis and additional comprehension of the underlying mechanisms is extremely necessary.

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Exploring and developing multifunctional intelligent biomaterials is crucial to improve next-generation therapies in tissue engineering and regenerative medicine. Recent findings show how distinct characteristics of in situ microenvironment can be mimicked by using different biomaterials. In vivo tissue architecture is characterized by the interconnection between cells and specific components of the extracellular matrix (ECM). Last evidence shows the importance of the structure and composition of the ECM in the development of cellular and molecular techniques, to achieve the best biodegradable and bioactive biomaterial compatible to human physiology. Such biomaterials provide specialized bioactive signals to regulate the surrounding biological habitat, through the progression of wound healing and biomaterial integration. The connection between stem cells and biomaterials stimulate the occurrence of specific modifications in terms of cell properties and fate, influencing then processes such as self-renewal, cell adhesion and differentiation. Recent studies in the field of tissue engineering and regenerative medicine have shown to deal with a broad area of applications, offering the most efficient and suitable strategies to neural repair and regeneration, drawing attention towards the potential use of biomaterials as 3D tools for in vitro neurodevelopment of tissue models, both in physiological and pathological conditions. In this direction, there are several tools supporting cell regeneration, which associate cytokines and other soluble factors delivery through the scaffold, and different approaches considering the features of the biomaterials, for an increased functionalization of the scaffold and for a better promotion of neural proliferation and cells-ECM interplay. In fact, 3D scaffolds need to ensure a progressive and regular delivery of cytokines, growth factors, or biomolecules, and moreover they should serve as a guide and support for injured tissues. It is also possible to create scaffolds with different layers, each one possessing different physical and biochemical aspects, able to provide at the same time organization, support and maintenance of the specific cell phenotype and diversified ECM morphogenesis. Our review summarizes the most recent advancements in functional materials, which are crucial to achieve the best performance and at the same time, to overcome the current limitations in tissue engineering and nervous tissue regeneration.

The progressive consumption growth of non-steroidal anti-inflammatory drugs (NSAIDs) has progressively raised the attention toward the gastrointestinal, renal, and cardiovascular toxicity. Increased risk of cardiovascular diseases was strictly associated with the usage of COX-2 selective NSAIDs. Other studies allowed to clarify that the cardiovascular risk is not limited to COX-2 selective but also extended to non-selective NSAIDs, such as Diclofenac and Ketoprofen. To date, although a less favorable cardiovascular risk profile for Diclofenac as compared to Ketoprofen is reported, the mechanisms through which NSAIDs cause adverse cardiovascular events are not entirely understood. The present study aimed to evaluate the effects of Ketoprofen in comparison with Diclofenac in immortalized human cardiomyocytes. The results obtained highlight the dose-dependent cardiotoxicity of Diclofenac compared to Ketoprofen. Despite both drugs induce the increase in ROS production, decrease of mitochondrial membrane potential, and proteasome activity modulation, only Diclofenac exposure shows a marked alteration of these intracellular parameters, leading to cell death. Noteworthy, Diclofenac decreases the proteasome 26S DC and this scenario may be dependent on the intracellular overload of oxidized proteins. The data support the hypothesis that immortalized human cardiomyocytes exposed to Ketoprofen are subjected to tolerable stress events, conversely Diclofenac exposition triggers cell death.