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Peer-reviewed veterinary case report

Plasma-activated solutions reverse chronic deltamethrin exposure induced intestinal injury via rebalancing redox homeostasis and counteracting cellular senescence.

Journal:
Scientific reports
Year:
2026
Authors:
Deng, Xiaoyuan et al.
Affiliation:
Department of Surgical Oncology · China
Species:
rodent

Abstract

Deltamethrin (DLM), a widely used pesticide, poses chronic exposure risks. Previous studies have shown its role in inducing intestinal mucosal barrier impairment. Meanwhile, plasma-activated solutions (PAS) ameliorate Dextran Sulfate Sodium (DSS)-induced colitis, primarily through the regulation of redox homeostasis. Building upon these findings, to further investigate the therapeutic potential of PAS against DLM-induced injury, we establish a chronic DLM exposure model in female BALB/c mice with concurrent free access to PAS. Intestinal tissues and serum are collected for H&E staining and measurement of serum inflammatory factors to assess inflammatory response. Immunofluorescence staining are used to detect intestinal injury and senescence. Reactive Oxygen Species (ROS) staining and glutathione (GSH) assays are performed to evaluate redox homeostasis. Results confirm that PAS effectively counteract chronic DLM-induced intestinal impairment, manifesting as restored body weight, decreased Disease Activity Index (DAI) scores, reduced apoptosis of intestinal epithelium and diminished inflammatory cell infiltration. To identify the key active component in PAS responsible for this therapeutic effect, A nitrogen-free PAS generator is used to produce nitric oxide-depleted PAS. Results show that after eight weeks of Nitro-Free PAS treatment, the therapeutic benefits are significantly weakened or disappeared. PAS mitigate chronic DLM induced intestinal impairment by rebalancing redox homeostasis, counteracting cellular senescence and restoring cell cycle progression. This therapeutic effect is mediated by reactive nitrogen species (RNS) within PAS.

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Original publication: https://pubmed.ncbi.nlm.nih.gov/41565719/