Hericium erinaceus is a valuable mushroom known for its strong bioactive properties. It shows promising potential as an excellent neuroprotective agent, capable of stimulating nerve growth factor release, regulating inflammatory processes, reducing oxidative stress, and safeguarding nerve cells from apoptosis. The active compounds in the mushroom, such as erinacines and hericenones, have been the subject of research, providing evidence of their neuroprotective effects. Further research and standardization processes for dietary supplements focused on H. erinaceus are essential to ensuring effectiveness and safety in protecting the nervous system. Advancements in isolation and characterization techniques, along with improved access to pure analytical standards, will play a critical role in achieving standardized, high-quality dietary supplements based on H. erinaceus. The aim of this study is to analyze the protective and nourishing effects of H. erinaceus on the nervous system and present the most up-to-date research findings related to this topic.

Platelets are anucleate cells derived from the megakaryocyte series, and have long been considered only as cells responsible for coagulation and the fibrinolysis process. However, recently more data shows that they are also effector cells in the inflammatory response and important elements of the immunological response. Platelets store and release many biologically active substances, including growth factors, cytokines and chemokines (tab. 1), which actively affect i.a. elements of the immune system, and thus become regulators of immunity and mediators of inflammatory response. Their impact on the immune system cells is also associated with the induction of leucocytes and progenitor cells to the site of pathogen permeation or vascular injury inflow, as well as endothelial cells. Interacting with neutrophils, monocytes and lymphocytes, they not only activate them, but also form platelet-leukocyte aggregates that immobilise pathogens and prevent their spreading. Furthermore, platelets are capable of absorbing pathogens, affecting anti-infection immunity of the system. It is also assumed that the presence of receptors on their surface, such as Toll-like receptors (TLRs), affects their initiation and activity of the immunological response.

The pathogenicity of RHDV (rabbit haemorrhagic disease virus) is mainly associated with its affinity to blood vessels, with causing disseminated intravascular coagulations (DIC), and with the stimulation of the host immune system. Moreover, there are implications suggesting that apoptosis may be a pivotal process in understanding the basis of viral haemorrhagic disease in rabbits - a serious infectious disease causing mortality to wild and domestic rabbits. The aim of this study is to evaluate, by means of flow cytometry, the dynamics of apoptosis in peripheral blood granulocytes and lymphocytes in rabbits experimentally infected with seven different strains of RHDV and so-called antigenic variants of RHDV denominated as RHDVa, i.e.: Hungarian 24V/89, 1447V/96, 72V/2003; Austrian 01-04, 237/04, V-412 and French 05-01. The results showed that all of the RHDV and RHDVa strains cause an increase in the number of apoptotic cells throughout the infection, which might indicate the need for further analysis of the importance of this process.

RHDV (rabbit haemorrhagic disease virus) is an etiologic factor of RHD (rabbit haemorrhagic disease), which is highly morbid and mortal viral infection of an adult European rabbit. Although three decades have passed since the first outbreak of rabbit haemorrhagic disease, the pathogenesis of RHD has still not been fully elucidated. It is known that RHDV replicates in the liver within the first hours following infection, causing necrotic and apoptotic cell death of hepatocytes. Anatomopathological changes are also observed in other organs of infected rabbits, i.e. lungs, spleen, kidneys, heart, as well as central nerve system. These changes leading to animals death are predominantly caused by systemic hemorrhagic diathesis with disseminated intravascular coagulation (DIC), appearing most likely as a consequence of liver cell loss through RHDV-induced apoptosis. In this paper, we presented previously described changes in biochemical and coagulation factors in RHDV infection.