Neuroinflammation plays a crucial role in the development of various neurological diseases, including neurodegenerative disorders, leading to significant neuronal dysfunction. Current treatments involve the use of non-steroidal anti-inflammatory drugs and steroids; however, they are associated with serious adverse effects, limiting their efficacy. Exploring natural products with anti-inflammatory properties appears promising, with resveratrol, a polyphenol found in various plants, standing out for its potential benefits. Studies on resveratrol and its anti-inflammatory properties have been increasing in recent years, and analyzing the profile of this knowledge area can bring benefits to the scientific community. Therefore, this study conducted bibliometric analyses, using “resveratrol AND neuroinflammation” as search terms in the Web of Science Core Collection database. The analysis, performed with VOSviewer software version 1.6.18, encompasses 323 publications. Key terms in the studies include “resveratrol”, “neuroinflammation”, and “oxidative stress”, with China leading in the number of publications. The Federal University of Rio Grande do Sul in Brazil emerges as the institution with the highest contribution, and a phase 2 clinical study on resveratrol was the most cited. These results provide an overview of the global research landscape related to resveratrol and neuroinflammation, aiding decision making for future publications and advancing scientific understanding in this field.

Background/Objectives: Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by motor and cognitive impairments due to dopaminergic neuron loss. The neurotoxin MPTP is commonly used to model PD, as it selectively targets these neurons. Quercetin (QU), a flavonoid with antioxidant properties, has shown neuroprotective potential, but its poor solubility limits clinical application. Nanoemulsions (NEQU) have emerged as a strategy to enhance its bioavailability and efficacy. Methods: To evaluate the neuroprotective and antioxidant effects of QU and NEQU, zebrafish larvae were exposed to MPTP (50 µM) and assessed for survival, locomotion (total distance traveled), morphological parameters, reactive oxygen species (ROS), lipid peroxidation (via MDA), and reduced glutathione (GSH) levels. Results: Only NEQU pre-treatment reversed MPTP-induced locomotor deficits. Both QU and NEQU (2.5 µM) significantly reduced ROS production and lipid peroxidation, with no effect on GSH levels. Notably, MPTP exposure led to a significant reduction in head size, an unprecedented finding in zebrafish PD models, indicating neurotoxicity. Morphometric analysis showed no change in total body length. However, MPTP significantly decreased swim bladder size and increased yolk sac size. Treatment with QU and NEQU attenuated these swim bladder alterations; no significant differences were observed in other parameters. Conclusions: These findings suggest that quercetin, particularly when nanoencapsulated, is a promising candidate for further development as a therapeutic agent to mitigate PD-related neurodegeneration.

Background/Objectives: Epilepsy is a common neurological condition characterized by the occurrence of a seizure. It affects around 50 million individuals worldwide, and despite the large quantity of anti-seizure medications available, 30% of epileptic patients still suffer from seizures. Therefore, it is necessary to find new therapeutic options. Interestingly, polydatin has shown promising effects on epilepsy treatment due to its antioxidant and anti-inflammatory properties. Thus, this study aimed to evaluate the effects of polydatin (200, 300, and 400 µM) on a pentylenetetrazol (PTZ)-induced seizure model in wild-type zebrafish (Danio rerio) larvae. Methods: Seizure-like behavior, cell death, reactive species (RS) production, and lipid peroxidation were analyzed. Results: Pre-treatment with polydatin at 200 and 300 µM did not have a significant impact on seizure occurrence and the behavior of animals exposed to PTZ. Diazepam decreased seizure occurrence and increased the latency to achieve each seizure stage. Exposure to PTZ increased the swimming activity, and this effect was suppressed by diazepam but not by polydatin. PTZ exposure increased the RS production, which was significantly attenuated by polydatin at 400 µM and DMSO. Cell death and lipid peroxidation were not changed when compared to the experimental groups. Conclusions: Only the experimental positive control (diazepam) showed anti-seizure effects. Therefore, we failed to observe any anti-seizure effects of polydatin using a zebrafish experimental model. However, we cannot rule out its effects in other experimental models and different treatment protocols.