Literature DB >> 31933850

Down-regulation of LncRNA UCA1 alleviates liver injury in rats with liver cirrhosis.

Yinhong Zhu1, Xiaobei Chen1, Chunhua Zheng1, Xianlin Rao1, Xiaomou Peng2.   

Abstract

OBJECTIVE: The purpose of this study is to explore the role of long non-coding RNA HULC (lncRNA HULC) in liver injury of rats with cirrhosis.
METHODS: The rat model of liver cirrhosis was induced by dimethylnitrosamine (DMN), which was intraperitoneally injected with siRNA-negative control (NC) or HULC siRNA. HULC expression in rat liver tissues was detected by qRT-PCR. The amounts of alanine transaminase (ALT) and aspartate aminotransferase (AST) in serum and levels of malonyldialdehyde (MDA) and superoxide dismutase (SOD) in liver tissues were measured. TUNEL staining was used to determine hepatocyte apoptosis. Western blot analysis was used to detect the expression of Caspase-3, Bax, and Bcl-2 in liver tissues. qRT-PCR and ELISA were used to detect the mRNA levels and contents of IL-1β and TNF-α in liver tissues and serum of rats, respectively.
RESULTS: High expression of HULC was found in liver tissues of rats with liver cirrhosis. Downregulation of HULC reduced the contents of ALT and AST in serum of rats, inhibited liver tissue lesions and liver fibrosis in rats, suppressed apoptosis (lower expression of caspase-3 and Bax as well as higher BCL-2 expression) of hepatocytes in rats, and inhibited oxidative stress (decreased MDA and increased SOD) and inflammatory injury (decreased IL-1β and TNF-α) in rats with cirrhosis.
CONCLUSION: The findings in this study highlight that the expression of HULC is up-regulated in liver tissues of rats with cirrhosis, and down-regulation of UCA1 could inhibit liver injury in rats with cirrhosis. IJCEP
Copyright © 2019.

Entities:  

Keywords:  Liver cirrhosis; UCA1; hepatocytes apoptosis; inflammatory injury; liver injury; oxidative stress

Year:  2019        PMID: 31933850      PMCID: PMC6945082     

Source DB:  PubMed          Journal:  Int J Clin Exp Pathol        ISSN: 1936-2625


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