Interleukin-24 protects against liver injury in mouse models

Autor: Ming-Shi Chang, Wei Chih Ho, Hsiao Hsuan Wang, Yu Hsiang Hsu, Min Hao Sue, Kung Chao Chang, Jian Hao Huang
Jazyk: angličtina
Rok vydání: 2021
Předmět:
Liver Cirrhosis
Male
0301 basic medicine
Interleukin-24
Liver fibrosis
lcsh:Medicine
Inflammation
Pharmacology
Protective Agents
Severity of Illness Index
General Biochemistry
Genetics and Molecular Biology
Cell Line
Mice
03 medical and health sciences
Liver disease
chemistry.chemical_compound
0302 clinical medicine
Thioacetamide-induced liver injury
Hepatic stellate cells
Interleukin 24
medicine
Humans
Animals
Receptor
Liver injury
lcsh:R5-920
business.industry
Interleukins
lcsh:R
General Medicine
medicine.disease
Immunohistochemistry
Disease Models
Animal
030104 developmental biology
chemistry
Apoptosis
030220 oncology & carcinogenesis
Hepatocytes
Commentary
Hepatic stellate cell
Disease Susceptibility
Chemical and Drug Induced Liver Injury
medicine.symptom
Thioacetamide
business
lcsh:Medicine (General)
Biomarkers
Research Paper
Zdroj: EBioMedicine, Vol 64, Iss, Pp 103213-(2021)
EBioMedicine
ISSN: 2352-3964
Popis: Background Interleukin-24 (IL-24) binds to two kinds of receptor complexes, namely IL-20R1/IL-20R2 and IL-20R2/IL-22R1, which are also bound by IL-20. IL-20 plays a detrimental role in liver fibrosis. Due to the sharing of receptor complexes, we aimed to determine whether IL-24 also participates in liver fibrosis. Methods Clinical biopsy specimens from various stages of liver fibrosis were used to analyze IL-24 expression. IL-24 protein was administered to mice with thioacetamide (TAA)-induced liver injury. The direct effects of IL-24 on mouse primary hepatocytes or hepatic stellate cells (HSCs) were analyzed. Wild-type, IL-20R1-, and IL20R2-deficient mice were used to establish a model of acute TAA-induced liver injury. Findings Among patients with more severe liver fibrosis, there was a reduced IL-24/IL-20 ratio. Administration of IL-24 protein protected mice from TAA-induced liver injury and reduction of liver inflammation by antioxidant effects. IL-24 protected hepatocytes from TAA-induced apoptosis and prevented liver fibrosis through the inhibition of the HSCs activation. The protective role of IL-24 acted on liver cells were mainly IL-20R1-independent. IL-20R2-deficient mice exhibited more severe liver injury upon TAA treatment, thus confirming the protective role of IL-24. Interpretation IL-24 plays a key protective role in the progression of liver injury and has therapeutic potential for treating liver injuries. Funding This work was supported by the Ministry of Science and Technology of Taiwan (MOST 106–2320-B-006–024) and Taiwan Liver Disease Prevention & Treatment Research Foundation.
Databáze: OpenAIRE
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