Silicosis has been topping the list of high-incidence occupational diseases in developing countries and cannot be completely cured. Recent advances in stem cell research have made possible the treatment of various diseases including lung fibrosis. The application of stem cell therapy in occupational diseases, in particular the use of adipose-derived mesenchymal stem cells (AD-MSCs) in treatment of silicosis, has not yet been reported. The aim of the study is to explore the intervening effect of silica-induced lung fibrosis in rats. In this study, we investigated the anti-pulmonary fibrosis effects of the transplantation of AD-MSCs in rats in which lung fibrosis was induced by oral tracheal intubation with silica suspension. Twenty rats were divided into four groups: control group (n = 5), exposure group (n = 5), vehicle group (n = 5) and treatment group (n = 5). AD-MSCs were given to rats after exposure to silica for 24 h. Twenty-eight days after AD-MSC transplantation, we examined the organ coefficient, inflammatory cytokines, apoptosis, pathological and fibrotic changes in lung tissue. Results showed that exposure to silica for 28 days induced an increase of the lung coefficient with significant pulmonary fibrosis. Treatment with AD-MSC transplantation led to a remissive effect on pulmonary fibrosis. We found that after AD-MSC transplantation the inflammatory response decreased and Caspase-3 protein expression significantly decreased with a significant increase of the Bcl-2/Bax ratio. Anti-inflammatory and anti-apoptosis of AD-MSCs may play important roles in their anti-pulmonary fibrosis effect. Our data suggest that transplantation of AD-MSCs holds promise for potential interference in the formation of silicosis through regulating inflammatory and apoptotic processes.

Pulmonary fibrosis induced by silica dust is an irreversible, chronic, and fibroproliferative lung disease with no effective treatment at present. Previous studies have shown that early intervention with bone marrow mesenchymal stem/stromal cells (BMSCs) has positive effect on anti-pulmonary fibrosis caused by silica dust. However, early intervention using BMSCs is not practical, and the therapeutic effects of BMSCs advanced intervention on pulmonary fibrosis have rarely been reported. In this study, we investigated the effects of advanced transplantation (on the 28th day after exposure to silica suspension) of BMSCs on an established rat model of pulmonary fibrosis. Sprague Dawley (SD) rats were randomly divided into four groups including (1) control group (n = 6) which were normally fed, (2) silica model group (n = 6) which were exposed to silica suspension (1 mL of 50 mg/mL/rat), (3) BMSC transplantation group (n = 6) which received 1 mL BMSC suspension (2 × 10⁶ cells/mL) by tail vein injection on the 28th day after exposure to silica suspension, and (4) BMSC-CM (conditioned medium) transplantation group (n = 6) which received CM from the same cell number by tail vein injection on the 28th day after exposure to silica suspension. On the 56th day after exposure to silica suspension, we used computed tomography (CT), hematoxylin and eosin (H&E), and Masson’s trichrome staining to evaluate the changes in lung tissue. We examined the expression of epithelial-mesenchymal transition (EMT) and Wnt/β-catenin pathway-related proteins in lung tissue using immunohistochemistry and western blotting. Successful construction of a pulmonary fibrosis model was confirmed by H&E and Masson’s trichrome staining on the 28th day after exposure to silica suspension. On the 56th day after exposure, pulmonary CT examination showed a relieving effect of BMSCs on silica-induced pulmonary fibrosis which was confirmed by H&E and Masson’s trichrome staining. Treatment of BMSCs increased the expression of epithelial marker proteins including E-cadherin (E-cad) and cytokeratin19 (CK19) and reduced the expression of fibrosis marker proteins including Vimentin (Vim) and α-Smooth actin (α-SMA) after exposure to silica suspension. Furthermore, we found that Wnt/β-catenin signaling pathway is abnormally activated in silica-induced pulmonary fibrosis, and exogenous transplantation of BMSCs may attenuate their expression. BMSC transplantation inhibits the EMT to alleviate silica-induced pulmonary fibrosis in rats and the anti-fibrotic effect potentially by attenuating Wnt/β-catenin signaling. ᅟ

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.

Iron is an indispensable element for the normal physiological function of the brain. In terms of neuronal metabolism, iron is involved in multiple critical biological processes such as oxygen transport, energy metabolism, DNA synthesis, neurotransmitter synthesis and myelin formation. Maintaining brain iron homeostasis is crucial for neurodevelopment and function. Iron dyshomeostasis has been associated with the onset and progression of various neuropsychiatric disorders, including Parkinson’s disease, Alzheimer’s disease, depression, schizophrenia, attention deficit hyperactivity disorder, and autism spectrum disorder. In neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease, abnormally elevated iron levels can be detected in specific brain regions, including the basal ganglia and the prefrontal cortex. These changes are often accompanied by pathological processes such as oxidative stress, neuroinflammation, and pathological protein aggregation. Therefore, brain iron metabolism is an important entry point for understanding the pathophysiological process of neuropsychiatric disorders. Mechanistically, iron overload induces oxidative damage through the Fenton reaction, exacerbating mitochondrial dysfunction and abnormal protein aggregation. The effects of iron deficiency vary across different diseases; its impact on myelination and neurotransmitter synthesis may increase the risk of neurodevelopmental disorders such as attention deficit hyperactivity disorder (ADHD), while its effects on immune activation and energy metabolism may contribute to the development of mental disorders such as depression. This article systematically reviews the current research progress of the role of cerebral iron metabolism in neuropsychiatric diseases. It focuses on the mechanisms underlying iron homeostasis imbalances in neurodegenerative and psychiatric diseases. Building on this foundation, the article analyzes the therapeutic targets and clinical significance of iron metabolism-related interventions and outlines future research directions in this field.