Decorin inhibits the formation of hard nodules after microwave ablation by inhibiting the TGF-β1/SMAD and MAPK signaling pathways: in a Bama miniature pig model of mammary gland hyperplasia

Benign breast lesions are often associated with hard nodule formation after microwave ablation (MWA), which persists for a long time and causes problems in patients. The aim of this study was to evaluate the efficacy of decorin in the treatment of hard nodule formation and its potential mechanism of...

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Veröffentlicht in:International journal of hyperthermia 2023-12, Vol.40 (1), p.2188151-2188151
Hauptverfasser: Du, Yue, Liu, Xinyao, Du, Kai, Zhang, Wenkai, Li, Rui, Yang, Lizhi, Cheng, Linggang, He, Wen, Zhang, Wei
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Sprache:eng
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Zusammenfassung:Benign breast lesions are often associated with hard nodule formation after microwave ablation (MWA), which persists for a long time and causes problems in patients. The aim of this study was to evaluate the efficacy of decorin in the treatment of hard nodule formation and its potential mechanism of action. Using a Bama miniature pig model of mammary gland hyperplasia, immunohistochemistry, Masson's trichrome and western blotting were firstly applied to compare the extent of fibrosis and activation of key members of the TGF-β1/SMAD and MAPK signaling pathways of hard nodule in the control and MWA groups, and then the extent of fibrosis and expression of signaling pathways in hard nodule were examined after application of decorin. The results showed that the MWA group had increased levels of TGF-β1, p-SMAD2/3, p-ERK1/2, and collagen I proteins and increased fibrosis at 2 weeks, 4 weeks, and 3 months after MWA. After decorin treatment, the expression levels of each protein were significantly downregulated, and the degree of fibrosis was reduced at 2 weeks, 4 weeks, and 3 months after MWA compared with the MWA group. In conclusion, these results suggest that activation of TGF-β1 may play an important role in hard nodule formation and that decorin may reduce hard nodule formation after MWA in a model of mammary gland hyperplasia by inhibiting the TGF-β1/SMAD and MAPK signaling pathways.
ISSN:0265-6736
1464-5157
DOI:10.1080/02656736.2023.2188151