Exposure to toluene diisocyanate (TDI) can cause pulmonary diseases such as asthma. Inhibition of high mobility group box 1 protein (HMGB1) has been found to be protective against the toxic effects of TDI on human bronchial epithelial (HBE) cells. Here, we evaluated the in vivo positive roles of HMGB1 in the TDI-caused asthma mice and explored its underlying mechanisms in HBE cells. We found that suppression of HMGB1 obviously alleviated airway inflammation, airway hyperresponsiveness, and airway remodeling in the lung tissue of the asthma mice. The in vitro results showed that inhibition of HMGB1 ameliorated TDI-induced reactive oxygen species (ROS) release, inflammatory response, and activation of autophagy in HBE cells. At the molecular level, inhibition of HMGB1 decreased the expressions of HMGB1, Toll-like receptor 4, Vimentin and matrix metalloproteinase-9 proteins, activated NF-κB and NOD-like receptor protein 3 (NLRP3) inflammasome, and increased E-cadherin expression. Importantly, activation of autophagy could lead to the overactivation of NLRP3 inflammasome in TDI-induced asthma. These results suggest that inhibition of HMGB1 can alleviate TDI-induced asthma through ROS/AMPK/autophagy pathways, which may provide valuable evidence for the pathogenesis and therapeutic targets of TDI-induced asthma.

The escalating crisis of plastic pollution has positioned microplastics (MPs) as globally pervasive environmental contaminants, with a documented presence across aquatic, terrestrial, and atmospheric ecosystems, as well as within biological organisms. A growing body of evidence suggests that MPs not only threaten ecological integrity but may also induce multifaceted neurotoxic effects in humans, particularly targeting the functional architecture of the prefrontal cortex (PFC). As the central regulator of cognition, emotional processing, and behavioral control, PFC dysfunction has been hypothesized to be associated with cognitive deficits, emotional dysregulation, and behavioral abnormalities. In this comprehensive review, we synthesize the current understanding of MP-mediated neurotoxicity through three interconnected pathways: (1) structural and functional impairment of PFC neural networks, (2) disruption of neurotransmitter homeostasis, and (3) potential associations with neuropsychiatric pathogenesis. By integrating these mechanistic insights, this work aims to provide a scientific foundation for risk assessment frameworks and evidence-based environmental health policies.