Up-regulation of microRNA-30b/30d cluster represses hepatocyte apoptosis in mice with fulminant hepatic failure by inhibiting CEACAM1
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Updated: Dec 27, 2025
Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method
Published on: October 23, 2018
Changpu Zhao1, Zhongqin Dang2, Junbo Sun3
1Internal Medicine Department, Henan University of Chinese Medicine, Zhengzhou, China.
Abstract:
Recently, impacts of microRNAs have been unraveled in human diseases, and we aimed to confirm the role of miR-30b/30d in fulminant hepatic failure (FHF). Expression of miR-30b/30d and CEACAM1 in serum of FHF patients and healthy people was measured by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis. Mice FHF models were established by injection of D-Galn and lipopolysaccharide, and were treated with miR-30b/30d mimics. Oxidative stress, liver injury, and inflammatory reaction in mouse liver tissues were measured using oxidative stress-related factor kits, hematoxylin-eosin staining and enzyme-linked immunosorbent assay, respectively. Moreover, cell cycle distribution and apoptosis of hepatocytes of mice were determined by flow cytometry, and the target relation between miR-30b/30d and CEACAM1 was confirmed by bioinformatic method and dual luciferase reporter gene assay. MiR-30b/30d expression was positively, and CEACAM1 expression was negatively related to prognosis of FHF patients. Up-regulation of miR-30b/30d attenuated oxidative stress, liver injury, and inflammatory reaction, and improved survival rate of FHF mice. Furthermore, elevated miR-30b/30d ameliorated apoptosis and cell cycle arrest of hepatocytes of FHF mice. CEACAM1 was a target gene of miR-30b/30d. This study highlights that up-regulated miR-30b/30d attenuates the progression of FHF by targeting CEACAM1, which may be helpful to FHF treatment.
Insights
MicroRNAs miR-30b/30d play a crucial role in treating fulminant hepatic failure (FHF). Upregulating miR-30b/30d can reduce liver injury and inflammation, offering a potential new therapy for FHF.
Area of Science:
- Biochemistry
- Molecular Biology
- Hepatology
Background:
- MicroRNAs (miRNAs) are increasingly recognized for their roles in human diseases.
- Fulminant hepatic failure (FHF) is a severe condition with high mortality.
- The specific involvement of miR-30b/30d in FHF pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the role of miR-30b/30d in fulminant hepatic failure (FHF).
- To explore the therapeutic potential of miR-30b/30d in FHF.
- To identify the molecular targets of miR-30b/30d in FHF.
Main Methods:
- Serum expression analysis of miR-30b/30d and CEACAM1 in FHF patients and controls using RT-qPCR and Western blot.
- Establishment of mouse FHF models and treatment with miR-30b/30d mimics.
- Assessment of liver injury, oxidative stress, inflammation, apoptosis, and cell cycle in mice.
- Bioinformatic analysis and dual luciferase reporter gene assay to confirm target gene interaction.
Main Results:
- miR-30b/30d expression was positively correlated with FHF patient prognosis, while CEACAM1 expression was negatively correlated.
- Upregulation of miR-30b/30d in a mouse model significantly attenuated liver injury, oxidative stress, and inflammation.
- miR-30b/30d mimics improved survival rates, reduced hepatocyte apoptosis, and alleviated cell cycle arrest in FHF mice.
- CEACAM1 was identified as a direct target gene of miR-30b/30d.
Conclusions:
- Upregulated miR-30b/30d demonstrates a protective effect against FHF progression.
- miR-30b/30d exerts its therapeutic effects by targeting CEACAM1.
- Targeting miR-30b/30d represents a promising therapeutic strategy for FHF treatment.
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