ArticlePloS one2026
TGF-β1 relieves burn injury induced pain by alleviating inflammation in mouse.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Potential targets of baicalein in macrophages revealed by bulk and single cell RNA sequencing analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
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9 authors.
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Abstract
Burn injuries are severe traumas characterized by tissue damage and inflammation, and pain is the common symptom of burn patients. Transforming growth factor beta 1 (TGF-β1) is a multifunctional cytokine involved in organ development, immune response, tumor biology and injury repair. This study investigates the effects of TGF-β1 on the burn injury induced pain and explore the underlying mechanisms. A mouse model of second degree burn injury was established, and spinal intrathecal injection with lentivirus was used to knockdown or overexpress TGF-β1. The assessment of mechanical allodynia and thermal hyperalgesia was adapted to evaluate the impact of TGF-β1 on the burn injury induced pain. The expressions of inflammatory factors were measured by using RT-qPCR, while immunofluorescence staining was employed to detect the effects of TGF-β1 on macrophage infiltration in the burned plantar skin. Western blot was used to analyze the effects of TGF-β1 on microglia, astrocytes and signal pathway. RT-qPCR results demonstrated that lentiviruses injection could knockdown or overexpress TGF-β1 in ipsilateral spinal cord, and reduce pro-inflammatory factors (IL-1β, IL-6 and TNF-α) expression and promote anti-inflammatory factor (IL-10) expression. The behavioral assessments revealed that TGF-β1 overexpression alleviated mechanical allodynia and thermal hyperalgesia. Immunofluorescence staining and Western blot revealed that TGF-β1 reduced the macrophage infiltration in the plantar skin, inhibited expressions of marker proteins of microglia and astrocyte, and promoted the phosphorylation of smad2. These findings suggested that TGF-β1 mitigated burn injury induced pain by attenuating inflammatory response via TGF-β1/smad2 pathway. This study provides an experimental and theoretical basis supporting the potential use of TGF-β1 as an anti-inflammatory and analgesic for burn injury.
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