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Inflammatory suppression and immunity regulation benefits of honokiol in a rat model of acute peritonitis via the regulation of NLRP3 inflammasome and Sirt1/autophagy axis.

التفاصيل البيبلوغرافية
العنوان: Inflammatory suppression and immunity regulation benefits of honokiol in a rat model of acute peritonitis via the regulation of NLRP3 inflammasome and Sirt1/autophagy axis.
المؤلفون: Pan X; Department of Emergency, Suichang People's Hospital, Lishui , PR China., Hua Z; Department of Nephrology, Suichang People's Hospital, Lishui, PR China., Fan G; Department of Breast Surgery, Suichang People's Hospital, Lishui, PR China., Feng Q; Intensive Care Unit, Quzhou Kecheng People's Hospital, Quzhou, PR China. qinglongfengicu@sina.com.
المصدر: Histology and histopathology [Histol Histopathol] 2024 Jul; Vol. 39 (7), pp. 921-934. Date of Electronic Publication: 2023 Dec 12.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Histology and Histopathology Country of Publication: Spain NLM ID: 8609357 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1699-5848 (Electronic) Linking ISSN: 02133911 NLM ISO Abbreviation: Histol Histopathol Subsets: MEDLINE
أسماء مطبوعة: Publication: Murcia : Histology and Histopathology
Original Publication: Murcia, Spain : Gutenberg, 1986-
مواضيع طبية MeSH: Sirtuin 1*/metabolism , NLR Family, Pyrin Domain-Containing 3 Protein*/metabolism , Autophagy*/drug effects , Peritonitis*/immunology , Peritonitis*/drug therapy , Inflammasomes*/metabolism , Lignans*/pharmacology , Lignans*/therapeutic use , Disease Models, Animal* , Biphenyl Compounds*/pharmacology , Biphenyl Compounds*/therapeutic use , Rats, Sprague-Dawley*, Animals ; Mice ; Rats ; RAW 264.7 Cells ; Male ; Acute Disease ; Inflammation ; Signal Transduction/drug effects ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Allyl Compounds ; Phenols
مستخلص: Background: NLRP3 inflammasome and Sirt1/autophagy axis are potential targets for advancing acute peritonitis (AP). Honokiol (HNK), a bioactive substance, has the potential to improve AP.
Materials and Methods: The AP model rats were established by cecal ligation and puncture (CLP). Rats were randomized into the Sham, Sham+HNK, CLP, and CLP+HNK groups. The therapeutic effects of HNK on organ infection, inflammation and immunity were observed in AP rats. The inflammation of RAW 264.7 cells was induced by lipopolysaccharide (LPS) and divided into the Control, HNK, LPS, and LPS+HNK groups. The effects of HNK on immunity and inflammation were observed. Moreover, the inflammatory cell model was further transfected with NLRP3 overexpressing plasmid, and the regulatory effect of HNK on NLRP3 in AP cells was detected.
Results: HNK treatment improved survival, biochemical indexes, and lung and kidney injury and inhibited inflammatory cytokine release and bacterial infection in CLP rats. In CLP rats and RAW 264.7 cells, HNK treatment improved the release of the CD4+ and CD8+ T cells, decreased the associated proteins' levels of the NLRP3 inflammasome, and activated the expression of proteins in the Sirt1/autophagy axis. It improved viability and reduced apoptosis and the degrees of TNF-α, IL-1β, and IL-6 mRNA in RAW 264.7 cells. In addition, HNK treatment antagonized the effect of NLRP3-overexpressed on inflammation and immunity.
Conclusions: HNK improved AP by inhibiting NLRP3 inflammasome and activating the Sirt1 autophagy axis in vivo and in vitro .
(©The Author(s) 2024. Open Access. This article is licensed under a Creative Commons CC-BY International License.)
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المشرفين على المادة: EC 3.5.1.- (Sirtuin 1)
0 (NLR Family, Pyrin Domain-Containing 3 Protein)
11513CCO0N (honokiol)
0 (Inflammasomes)
0 (Lignans)
EC 3.5.1.- (Sirt1 protein, rat)
0 (Biphenyl Compounds)
0 (Nlrp3 protein, rat)
0 (Anti-Inflammatory Agents)
0 (Allyl Compounds)
0 (Phenols)
تواريخ الأحداث: Date Created: 20231219 Date Completed: 20240624 Latest Revision: 20240624
رمز التحديث: 20240624
DOI: 10.14670/HH-18-688
PMID: 38112214
قاعدة البيانات: MEDLINE
الوصف
تدمد:1699-5848
DOI:10.14670/HH-18-688