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Introduction Ozone (O3) is one of the most prevalent atmospheric pollutants, arising from a photochemical reaction between volatile organic compounds (VOC), nitrogen oxides (NOx), and sunlight. O3 triggers oxidative stress, resulting in lipid oxidation, inflammation, alterations in metabolic and cellular signaling, and potentially initiating cell death in vulnerable brain regions. Inflammation and oxidative stress are recognized for their ability to induce cell death, primarily through the apoptosis pathway, involving various proteins that participate in this process via two pathways: intrinsic and extrinsic. Objective This study aims to identify the expression of pro-apoptotic proteins and Bcl-2 in the frontal cortex, cerebellum, and hippocampus of rats exposed to O3 acutely. Methods Two groups of 20 Wistar rodents (250-300 g) were established. The control group (n=10) was exposed to unrestricted polluted air for 12 hours, while the experimental group (n=10) was exposed to 1 ppm of O3. After exposure, the animals were sacrificed for immunofluorescence and Western blot analysis. Using a t-test, the arbitrary units of pro-apoptotic proteins and Bcl-2 were compared between the two groups. Results Significant increases in caspase-8 and caspase-3 activation were found in the O3-exposed group compared to the control group, specifically in the frontal cortex, cerebellum, and hippocampus. Additionally, notable changes in Bcl-2 expression were observed in these brain regions. The TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) assay further indicated significant differences in immunopositivity between the groups in the same areas. However, intrinsic apoptotic proteins such as Bax, VDAC1, and cytochrome-c did not show significant differences between the groups within these structures. Western blot analyses aligned with the immunofluorescence results, showing statistically significant concentrations of caspase-8 in the cerebellum, caspase-3 in the hippocampus, and Bcl-2 in the frontal cortex in the O3 exposed group. Conversely, proteins like Bax, cytochrome-c, and VDAC1 did not exhibit significant differences in all analyzed structures. Conclusions This study demonstrates that acute exposure to 1 ppm of ozone can trigger neuronal apoptosis in the frontal cortex, hippocampus, and cerebellum of rats, primarily through the activation of the extrinsic apoptosis pathway via caspase-8 and caspase-3. Additionally, it causes a reduction in Bcl-2 expression, an essential antiapoptotic protein. Despite not observing the activation of intrinsic pathway proteins like BAX, VDAC, or cytochrome-c, the study suggests that chronic O3 exposure might promote cell death by activating this pathway, requiring further long-term research.
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Epilepsy stands as a prominent neurological disorder, affecting a substantial number of individuals who, unfortunately, do not respond to conventional antiepileptic medications. To unravel the intricate mechanisms underlying epileptic seizures and explore potential therapeutic avenues, researchers have turned to animal models. Among these models, rats have emerged as one of the cornerstones of epilepsy research. This bibliometric analysis embarks on the crucial task of delving into the role of rat models in deciphering the mysteries of epileptic seizures and, notably, pinpointing the most prevalent models in use. Our study harnessed Scopus' citation tracking feature to review a range of research papers dating from 1969 to 2020, all dedicated to the exploration of epileptic seizures in rats. The citations that emerged from this rigorous process were subjected to thematic coding, primarily centered around the specific epileptic animal models employed, and subsequently, comprehensive descriptive statistics were computed. In this effort, we found a total of 1,318 publications that explore the world of rat studies, accumulating a substantial citation count of 44,824 references. This analysis illuminated the invaluable role that research employing rat models has played in shaping our current clinical understanding of epileptic seizures. Notably, several models have emerged as predominant forces in this field, including those induced by pilocarpine, pentylenetetrazole (PTZ), kainic acid (KA), electric kindling, and electroshock. This bibliometric exploration serves as a resounding reminder of the pivotal position that rat models occupy in advancing our comprehension of epilepsy. These findings resonate strongly, underscoring the continued importance of directing research and development funding toward this debilitating disorder, with the ultimate aim of maximizing the benefits for the patients grappling with this condition. The potential to revolutionize our approach to epilepsy and enhance the quality of life for those affected remains a beacon of hope, illuminated by the contributions of these tireless researchers and their trusty rat companions.
