Grazing, as an important land use method in grassland, has a significant impact on the morphological and physiological traits of plants. However, little is known about how the molecular mechanism of plant responds to different grazing intensities. Here, we investigated the response of Taraxacum mongolicum to light grazing and heavy grazing intensities in comparison with a non-grazing control. Using de novo transcriptome assembly, T. mongolicum leaves were compared for the expression of the different genes under different grazing intensities in natural grassland. In total, 194,253 transcripts were de novo assembled and comprised in nine leaf tissues. Among them, 11,134 and 9058 genes were differentially expressed in light grazing and heavy grazing grassland separately, with 5867 genes that were identified as co-expression genes in two grazing treatments. The Nr, SwissProt, String, GO, KEGG, and COG analyses by BLASTx searches were performed to determine and further understand the biological functions of those differentially expressed genes (DEGs). Analysis of the expression patterns of 10 DEGs by quantitative real-time RT-PCR (qRT-PCR) confirmed the accuracy of the RNA-Seq results. Based on a comparative transcriptome analysis, the most significant transcriptomic changes that were observed under grazing intensity were related to plant hormone and signal transduction pathways, carbohydrate and secondary metabolism, and photosynthesis. In addition, heavy grazing resulted in a stronger transcriptomic response compared with light grazing through increasing the of the secondary metabolism- and photosynthesis-related genes. These changes in key pathways and related genes suggest that they may synergistically respond to grazing to increase the resilience and stress tolerance of T. mongolicum. Our findings provide important clues for improving grassland use and protection and understanding the molecular mechanisms of plant response to grazing.

Microplastics (MPs) are emerging pollutants with pervasive respiratory exposure routes, yet their lung-specific toxicity mechanisms remain poorly defined. This study aims to investigate the size-dependent detrimental effects on pulmonary systems using in vivo (mice) and in vitro (coculture) models, simulating acute (single dose) and subchronic (28-day) exposures. Crucially, we identify epithelial-mesenchymal transition (EMT) as a novel cytotoxic mechanism and delineate the ECM-MMP signaling cascade as the primary driver of PS-MP-induced lung injury. In vivo, acute intratracheal exposure to 12 mg/kg PS-MPs (with 1 µm particles) resulted in weight loss (9.09 % vs. controls). PS-MPs accumulated dominantly in lungs, with 1 µm particles depositing 1.38-fold higher than 10 µm particles (quantitative result). Subchronic exposure (8 mg/kg) triggered particle-size-dependent pathology. 1 µm PS-MPs increased lung injury scores by 2.5-fold vs. 10 µm. Myeloperoxidase (MPO) and malondialdehyde (MDA) rose by 2.13-fold (1 µm) vs. 1.81-fold (10 µm). In vitro, 1 µm PS-MP-exposed lung cells induced mitochondrial depolarization (ΔΨm loss: 50 %) and apoptosis (17 % increase). Critically, 1 µm PS-MPs potently activated MMPs (MMP-2↑180 %, MMP9↑250 %) via ECM-MMP dysregulation. Our findings reveal that PS-MPs drive lung injury through oxidative stress, cell apoptosis, and mitochondrial dysfunction in a strict size-dependent manner (1 µm > 5 µm > 10 µm), with the ECM-MMP axis as a central pathway. The signaling pathway activated by PS-MPs in lung injury suggested that PS-MPs induced proliferation inhibition, oxidative stress, and EMT via activating the ECM-MMP signaling cascade. In addition, EMT activation suggested a novel mechanism for the cytotoxicity of PS-MPs, hinting at the potential carcinogenic effect of these pollutants.

The present study aimed to investigate the influence of guar gum supplementation in high-fat diets on the growth performance and intestinal oxidative stress, inflammation, and apoptosis of juvenile largemouth bass. Five isonitrogenous diets were prepared: a control diet (10% crude lipid, C), a high-fat diet (17% crude lipid, HF), and three high-fat diets supplemented with 0.3% guar gum (GG0.3), 1% guar gum (GG1), and 3% guar gum (GG3). Largemouth bass (3.1±0.2 g) were randomly assigned to fifteen tanks (30 fish/tank) and fed for 8 weeks. The results demonstrated that GG0.3 significantly increased specific growth rate (SGR) and increased feed conversion ratio (FCR) compared to HF (P < 0.05). For histology, high-fat diets containing guar gum significantly increased intestinal villus length, villus width, and perimeter ratio, compared with HF (P < 0.05). Compared with Control, HF significantly decreased reduced glutathione (GSH) contents and increased malondialdehyde (MDA) contents in the intestine (P < 0.05). Additionally, HF significantly increased the expression of interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α), and cysteine-aspartic proteases 9 (Caspase 9) in the intestine (P < 0.05). Compared to HF, GG0.3 significantly decreased MDA contents, increased GSH contents, and downregulated the expression of IL-1β, TNF-α, and Caspase 3 than diet HF in the intestine (P < 0.05). These results suggest that guar gum can alleviate the adverse effects of high-fat diets on growth and gut health in fish.