In the last decades, marine macroalgae have drawn attention mainly because of their bioactive constituents. Most brown algae are distributed over coastal areas of the Atlantic Ocean, Mediterranean Sea, Aegean Sea and Black Sea, and their composition varies with endogenous and exogenous factors. Phlorotannins, fatty acids, sterols and carbohydrates are some of the compounds responsible for biological activities related to cytotoxic, antiviral, antifungal, antibacterial, antidiabetic, antioxidant and anti-inflammatory potential. In this review we seek to highlight some of the compounds responsible for these last two biological activities, which have enormous importance for the management of neurodegenerative diseases, such as Alzheimer and Parkinson’s, with neuroinflammation and oxidative stress as hallmarks. However, one of the major problems associated with treating these diseases is the highly selective blood-brain-barrier, which can be overcome with nanocarriers used as delivery systems. Weighing the risks, benefits and toxicity of the used nanoparticles is nevertheless important. We also discuss zebrafish as an upcoming adequate biological model for in vivo screening of risks and benefits of such treatment strategies. This review aims to enable researchers working in the exploitation of these macroalgae and in the use of nanocarriers to potentiate the controlled delivery of bioactive compounds.

Addressing disease remission and treatment adherence in inflammatory bowel diseases (IBDs), such as Crohn’s disease, poses significant challenges due to underlying oxidative and inflammatory processes. Nanotechnology emerges as a promising avenue for enhancing therapeutic outcomes in IBD by optimizing drug bioactivity, reducing toxicity, and extending circulation time. Gold nanoparticles, known for their resistance to gastrointestinal pH and possessing antioxidant and anti-inflammatory properties, offer particular promise. They can be produced by green synthesis with seaweed Ericaria selaginoides (ES), itself associated with gastroprotective and anti-inflammatory activities. In a murine model of Crohn’s disease induced with 8% acetic acid, pretreatment with dexamethasone (0.2 mL/30 g) or Au@ES (25 and 50 mg/kg) effectively mitigated inflammatory features. Notably, ES (50 mg/kg) and Au@ES (50 mg/kg) administration resulted in significant reductions in both macroscopic and microscopic inflammation scores compared to the disease control group. Furthermore, these treatments normalized inflammatory cytokine expression while safeguarding myenteric plexus glial cells. They also impeded neutrophil activation, leading to reduced myeloperoxidase activity and lipid peroxidation, coupled with increased glutathione levels. In conclusion, ES and Au@ES exhibit potent efficacy in counteracting inflammation and oxidation processes in an experimental Crohn’s disease model, suggesting their potential as alternative therapeutic strategies for IBD.