دورية أكاديمية
Mechanism of sodium butyrate, a metabolite of gut microbiota, regulating cardiac fibroblast transdifferentiation via the NLRP3/Caspase-1 pyroptosis pathway
| العنوان: | Mechanism of sodium butyrate, a metabolite of gut microbiota, regulating cardiac fibroblast transdifferentiation via the NLRP3/Caspase-1 pyroptosis pathway |
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| المؤلفون: | Tiancheng Dong, Dingkao Huang, Zhengzheng Jin |
| المصدر: | Journal of Cardiothoracic Surgery, Vol 19, Iss 1, Pp 1-10 (2024) |
| بيانات النشر: | BMC, 2024. |
| سنة النشر: | 2024 |
| المجموعة: | LCC:Surgery LCC:Anesthesiology |
| مصطلحات موضوعية: | Gut microbiota metabolite sodium butyrate, Cardiac fibroblasts, Myofibroblasts, NLRP3 inflammasomes, Caspase-1, Cell pyroptosis, Surgery, RD1-811, Anesthesiology, RD78.3-87.3 |
| الوصف: | Abstract Background Cardiac fibroblasts (CFs) are activated after initial injury, and then differentiate into myofibroblasts (MFs), which play a pivotal role as the primary mediator cells in pathological remodeling. Sodium butyrate (NaB), being a metabolite of gut microbiota, exhibits anti-inflammatory property in local therapies on sites other than the intestine. Thus, this study aimed to probe the mechanism by which NaB regulates CFs transdifferentiation through the NLRP3/Caspase-1 pyroptosis pathway. Methods CFs were cultured in vitro and induced into MFs by TGFβ1. CFs were identified by immunofluorescence labelling technique of vimentin and α-SMA, followed by treatment with NaB or NLRP3 inflammasome inhibitor (CY-09) and its activator [nigericin sodium salt (NSS)]. The expression levels of α-SMA, GSDMD-N/NLRP3/cleaved Caspase-1 proteins, and inflammatory factors IL-1β/IL-18/IL-6/IL-10 were determined using immunofluorescence, Western blot and ELISA. Cell proliferation and migration were evaluated using the CCK-8 assay and the cell scratch test, respectively. Results Following the induction of TGFβ1, CFs exhibited increased expression levels of α-SMA proteins and IL-6/IL-10, as well as cell proliferative and migratory abilities. TGFβ1 induced CFs to differentiate into MFs, while NaB inhibited this differentiation. NaB inactivated the NLRP3/Caspase-1 pyroptosis pathway. CY-09 demonstrated inhibitory effects on the NLRP3/Caspase-1 pyroptosis pathway, leading to a reduction in TGFβ1-induced CFs transdifferentiation. NSS activated the NLRP3/Caspase-1 pyroptosis pathway, and thus partially counteracting the inhibitory effect of intestinal microbiota metabolite NaB on CFs transdifferentiation. Conclusion NaB, a metabolite of the gut microbiota, inhibited the activation of the NLRP3/Caspase-1 pyroptosis pathway in TGFβ1-induced CFs, repressed the transdifferentiation of CFs into MFs. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 1749-8090 |
| العلاقة: | https://doaj.org/toc/1749-8090Test |
| DOI: | 10.1186/s13019-024-02692-0 |
| الوصول الحر: | https://doaj.org/article/094c8a546b354fb6a6e2e361ff4eb423Test |
| رقم الانضمام: | edsdoj.094c8a546b354fb6a6e2e361ff4eb423 |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 17498090 |
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| DOI: | 10.1186/s13019-024-02692-0 |