Extracellular vesicles derived from Pinctada martensii mucus regulate skin inflammation via the NF-κB/NLRP3/MAPK pathway

BackgroundRadiodermatitis (RD) is an inflammatory lesion of skin mucosa caused by radiation, which causes itching and pain in patients' skin. Hypericum sampsonii has an anti‐inflammatory effect. This study aims to explore the potential effect and mechanism of H. sampsonii on RD.Materials and MethodsThe RD model was established using X‐ray irradiation of mice and the pain response of mice under different treatment methods. Serum levels of IL‐1β, IL‐6, and TNF‐α were measured by ELSA. The RD cell model was constructed by RAW264.7 cell, H. sampsonii intervention was conducted, and the changes of the NLRP3 inflammasome in the cells were detected by qRT‐PCR. The cells were stimulated with LPS and the protein changes of TLR4/NF‐κB were investigated by Western Blotting.ResultsH. sampsonii can better improve the skin status of RD mice, relieve pain, and reduce the secretion of serum inflammatory factors IL‐1β, IL‐6, and TNF‐α. H. sampsonii significantly down‐regulated the expression of NLRP3, Caspase‐1, pro IL‐1β, and IL‐1β. Lps‐induced activation of the TLR4/NF‐κB pathway promotes the expression of NLRP3 and pro‐IL‐1β, and H. sampsonii can inhibit this promotion.ConclusionH. sampsonii may inhibit NLRP3 inflammatory vesicle activation via interfering with TLR4/NF‐κB signaling to reduce the inflammatory response in macrophages and thus play a role in the treatment of RD.

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Extracellular vesicles derived from Pinctada martensii mucus regulate skin inflammation via the NF-κB/NLRP3/MAPK pathway

Cited by 3 publications

References 45 publications

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Hypericum sampsonii ameliorates radiodermatitis by inhibiting NLRP3 inflammasome activation

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