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Resolvin D1 promotes the resolution of inflammation in the ACLF rat model by increasing the proportion of Treg cells.
Chen, Linjun; Huang, Yixuan; Chen, Yizhen; Chen, Jiaxuan; You, Xueye; Zou, Laiyu; Chen, Jiabing; Chen, Zhixin; Wang, Xiaozhong; Huang, Yuehong.
Afiliación
  • Chen L; Department of Infectious Disease, Fujian Medical University Union Hospital, Fuzhou, China.
  • Huang Y; Department of Gastroenterology, Fujian Institute of Digestive Disease, Fujian Medical University Union Hospital, Fuzhou, China.
  • Chen Y; Department of Gastroenterology, Fujian Institute of Digestive Disease, Fujian Medical University Union Hospital, Fuzhou, China.
  • Chen J; Department of Internal Neurology, Fujian Medical University Union Hospital, Fuzhou, China.
  • You X; Department of Pathology, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
  • Zou L; Department of Infectious Disease, Fujian Medical University Union Hospital, Fuzhou, China.
  • Chen J; Department of Gastroenterology, Fujian Institute of Digestive Disease, Fujian Medical University Union Hospital, Fuzhou, China.
  • Chen Z; Department of Gastroenterology, Fujian Institute of Digestive Disease, Fujian Medical University Union Hospital, Fuzhou, China.
  • Wang X; Department of Gastroenterology, Fujian Institute of Digestive Disease, Fujian Medical University Union Hospital, Fuzhou, China.
  • Huang Y; Department of Gastroenterology, Fujian Institute of Digestive Disease, Fujian Medical University Union Hospital, Fuzhou, China.
Immun Inflamm Dis ; 11(11): e1076, 2023 Nov.
Article en En | MEDLINE | ID: mdl-38018579
OBJECTIVE: Acute-on-chronic liver failure (ACLF) causes organ system failures in patients and increases the risk of mortality. One of the main predictors of ACLF development in patients is the severity of systemic inflammation. The purpose of this study was to explore the effects of resolvin D1 (RvD1) on the rat model of ACLF. METHODS: The ACLF rats were induced by first intraperitoneally (ip) injecting CCl4 and porcine serum for 6 weeks to establish the chronic liver injury, followed by once administration (ip) of lipopolysaccharide and d-galactose d-GalN to cause acute liver injury (ALI). An hour before the ALI-induced treatment, rats were administrated (ip) with 0.9% saline or different doses of RvD1 (0.3 or 1 µg/kg). Afterward, the control and treated rats were killed and samples were collected. Biochemical analysis, hematoxylin-eosin and Sirius red staining, flow cytometry assay, and real-time polymerase chain reaction were used to assess the rat liver histopathological injury, the percentage of Treg cells in the spleen, and the messenger RNA (mRNA) levels of transcription factors and immunologic cytokines in liver. RESULTS: The necroinflammatory scores and the serum levels of transaminase significantly increased in ACLF rats compared with those in control rats. These impaired changes observed in ACLF rats could be attenuated by the administration of a low dose of RvD1 before the induction of ALI, which was associated with the increased proportion of regulatory T cells (Treg) in the spleen together with the increased gene expression ratio of Foxp3/RORγt and decreased mRNA level of Il-17a and Il-6 in the liver. CONCLUSION: A low dose of RvD1 can promote the resolution of inflammation in ACLF rats by increasing the proportion of Treg cells. RvD1, therefore, may be used as a potential drug for the treatment of patients with ACLF.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Linfocitos T Reguladores / Insuficiencia Hepática Crónica Agudizada Límite: Animals / Humans Idioma: En Revista: Immun Inflamm Dis Año: 2023 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Linfocitos T Reguladores / Insuficiencia Hepática Crónica Agudizada Límite: Animals / Humans Idioma: En Revista: Immun Inflamm Dis Año: 2023 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido