Air pollution caused by particulate matter (PM) poses an imminent threat to the global environment and public health. However, balancing the removal efficiency and pressure drop of most filter materials is difficult. Moreover, filter materials are non-degradable and non-recyclable, causing serious harm to the environment. Herein, a strategy to create fully degradable branched poly (lactic acid) (PLA) nanofibers based on electrospinning by adjusting the spinning solution properties was reported and branched PLA nanofibers were applied as nanofiber filter paper for air filtration materials. When the PLA and tetrabutylammonium chloride concentrations were 8 and 5 wt%, respectively, PLA nanofibers with branched structures were obtained. The obtained nanofibers possessed a small pore size (0.70 μm), high porosity (92.3%), appropriate mechanical properties, resulting in high PM 0.3 removal efficiency (99.95%), low air resistance (79.67 Pa), and promising long-term PM 2.5 purification. Notably, branched T-PLA-5 nanofibers exhibited excellent filtration performance when applied to cellulose wood pulp paper. The filtration efficiency of the nanofiber filter paper remained stable above 85% for PM 0.3 (32 L min À1 ) after 5000 backflushings. Thus, the preparation of such nanomaterials may provide new insights into the design and development of high-performance degradable filtration materials for various applications.
Aflatoxin B1 (AFB1) is a toxic food/feed pollutant, exerting extensive deleterious impacts on the liver. Oxidative stress and inflammation are considered to be vital contributors to AFB1 hepatotoxicity. Polydatin (PD), a naturally occurring polyphenol, has been demonstrated to protect and/or treat liver disorders caused by various factors through its antioxidant and anti-inflammatory properties. However, the role of PD in AFB1-induced liver injury is still elusive. Therefore, this study was designed to investigate the protective effect of PD on hepatic injury in mice subjected to AFB1. Male mice were randomly divided into three groups: control, AFB1 and AFB1-PD groups. The results showed that PD protected against AFB1-induced hepatic injury demonstrated by the reduced serum transaminase activity, the restored hepatic histology and ultrastructure, which could be attributed to the enhanced glutathione level, the reduced interleukin 1 beta and tumor necrosis factor alpha concentrations, the increased interleukin 10 expression at transcriptional level and the up-regulated mRNA expression related to mitophagy. In conclusion, PD could alleviate AFB1-induced hepatic injury by reducing oxidative stress, inhibiting inflammation and improving mitophagy.
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