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Published on: December 30, 2021
SIRT1 suppresses burn injury-induced inflammatory response through activating autophagy in RAW264.7 macrophages
Fu Han1, Zhenzhen Li1, Shichao Han1
1Department of Burns and Cutaneous Surgery, Fourth Military Medical University, Xi'an, Shaanxi, China.
Abstract:
The present study sought to investigate the association between silent information regulator 1 (SIRT1) and autophagy during systemic inflammatory response syndrome following burn injury. The experimental burn model in mice and macrophages were established. SIRT1 mRNA expression was quantified by quantitative real-time PCR. The protein levels of SIRT1 and the conversion of light chain 3 (LC3)-I to LC3-II were determined by western blot analysis. The formation of autophagosomes was assessed by green fluorescence protein-tagged LC3 fluorescence. The contents of inflammatory cytokines interleukin (IL)-1, IL-6, IL-10 and IL-18 were measured by ELISA. SIRT1 was highly expressed in burned tissues and RAW264.7 cells treated with serum obtained from mice with burn injuries. Moreover, SIRT1 overexpression augmented, whereas sirtinol, an inhibitor of SIRT1, attenuated burn injury-induced increasing number of autophagosomes and expression levels of LC3-II/LC3-I in RAW264.7 cells. Besides, sirtinol effectively prevented SIRT1-induced pro-inflammation during burn injury. Furthermore, autophagy inhibition by 3-methyladenine significantly attenuated SIRT1 overexpression-mediated pro-inflammatory cytokine production. SIRT1 abolished burn injury-induced inflammatory response by inducing autophagy.
Insights
Silent information regulator 1 (SIRT1) promotes autophagy, a cellular process, to reduce inflammation following burn injuries. This study shows SIRT1 protects against burn-induced inflammatory responses by activating autophagy.
Area of Science:
- Molecular Biology
- Immunology
- Cellular Biology
Background:
- Systemic inflammatory response syndrome (SIRS) is a critical complication of burn injuries.
- The role of silent information regulator 1 (SIRT1) and autophagy in burn-induced SIRS requires further elucidation.
Purpose of the Study:
- To investigate the association between SIRT1 and autophagy in the context of burn injury-induced SIRS.
- To determine the mechanism by which SIRT1 influences inflammatory responses post-burn.
Main Methods:
- Established experimental burn models in mice and utilized RAW264.7 macrophage cell line.
- Quantified SIRT1 mRNA via qRT-PCR and protein levels via Western blot.
- Assessed autophagy markers (LC3-I/LC3-II conversion, autophagosome formation) and inflammatory cytokines (IL-1, IL-6, IL-10, IL-18) using fluorescence microscopy and ELISA.
Main Results:
- SIRT1 expression was significantly upregulated in burned tissues and serum-exposed macrophages.
- SIRT1 overexpression enhanced autophagy, while its inhibition (sirtinol) attenuated burn-induced autophagy and inflammation.
- Autophagy inhibition counteracted SIRT1-mediated pro-inflammatory cytokine production.
Conclusions:
- SIRT1 plays a crucial role in modulating autophagy during burn injury-induced SIRS.
- SIRT1 exerts protective effects against burn-induced inflammation by inducing autophagy.
- Targeting SIRT1-autophagy pathway may offer therapeutic potential for managing burn-related inflammatory conditions.
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