OXIDATIVE STRESS AND NEUROINFLAMMATION MECHANISMS IN RAT BRAIN INDUCED BY PM₂.₅ EXPOSURE

Abstract

Exposure to fine particulate matter (PM₂.₅) has been associated with various health disorders, including its impact on the nervous system. Animal studies, particularly those using rodents, provide a controlled platform to explore the pathophysiological mechanisms underlying PM₂.₅-induced neurotoxicity. This study presents a systematic review of 15 peer-reviewed articles retrieved from academic databases, focusing on the effects of PM₂.₅ on the rat brain across four key aspects: (1) the impact of exposure on brain health, (2) mechanisms of oxidative stress and neuroinflammation, (3) the influence of combined exposure with other factors, and (4) the potential of therapeutic interventions to mitigate adverse effects. The analysis reveals that PM₂.₅ exposure contributes to neuroinflammation, oxidative stress, and cognitive dysfunction, marked by increased beta-amyloid protein levels, microglial activation, and disruption of the blood-brain barrier through multiple molecular pathways. Furthermore, interactions between PM₂.₅ and additional factors—such as high-cholesterol diets and co-exposure to pollutants like formaldehyde—can exacerbate neurotoxic effects synergistically. Several antioxidant compounds, including melatonin, vitamin E, and herbal extracts such as red ginseng and baicalin-geniposide, have demonstrated protective potential by modulating neuroinflammatory pathways and restoring cognitive function. This review underscores the need for further research into the long-term effects of PM₂.₅ exposure and the development of more effective antioxidant- and neuroinflammation-based intervention strategies to mitigate the risk of air pollution-induced neurodegenerative disorders.