Overexpression of C‑sis inhibits H2O2‑induced Buffalo rat liver cell apoptosis in�vitro and alleviates liver injury in a rat model of fulminant hepatic failure

Abstract

The present study aimed to investigate the role of the C-sis gene in the apoptosis of hepatocytes in vitro and in the liver function of a rat model of fulminant hepatic failure (FHF). Buffalo rat liver (BRL) cells were treated with hydrogen peroxide (H2O2) to induce apoptosis and then transfected with a C-sis overexpression vector. A rat model of FHF was established, and C-sis was overexpressed. The mRNA and protein expression of C-sis were examined using reverse transcription-polymerase chain reaction and western blot analyses, respectively. Cell viability was assessed by CCK8, and a TUNEL assay was used to examine cell apoptosis. Flow cytometry was used for cell cycle detection. Hematoxylin and eosin staining was used for histological examination. The levels of alanine transaminase (ALT) and aspartate transaminase (AST) were also examined in the rats. The results showed that C-sis was successfully overexpressed in the cells and rat model. Compared with H2O2-treated BRL cells, the overexpression of C-sis significantly inhibited cell apoptosis, promoted cell viability, and decreased the expression of cleaved caspase-3. Similar results were observed in the FHF rats treated with the C-sis overexpression plasmid, compared with those treated with empty plasmids. In addition, in the FHF rats overexpressing C-sis, histological examination showed that liver injury was alleviated, the levels of ALT and AST were significantly decreased, and mortality rate was significantly decreased, compared with those observed in the rats treated with empty plasmids. In conclusion, the overexpression of C-sis inhibited the H2O2-induced apoptosis of BRL cells in vitro, and alleviated liver injury, improved liver function, and decreased mortality rates in rat models of FHF.

Milk‑derived hexapeptide PGPIPN prevents and attenuates acute alcoholic liver injury in mice by reducing endoplasmic reticulum stress

“…The main metabolism of alcohol (~90%) occurs in the liver, and the liver is injured after heavy drinking, which results in an increase in hepatocyte permeability due to cellular oxidative stress or damage ( 33 ). ALT and AST are mainly present in the mitochondria of hepatocytes ( 34 ). When hepatocytes are broken due to AALI, ALT and AST of hepatocytes are rapidly released into the blood, resulting in an increase in serum ( 35 , 36 ).…”

Oxidative Stress and Apoptosis Contributed to Nonylphenol-Induced Cell Damage in Mouse NCTC Clone 1469 Cells

“…LDH, ALT, and AST are important intracellular enzymes, which are indicators of liver cell damage [24,25]. After NCTC Clone 1469 was cultured with various concentrations of NP for 12 h, the activities of LDH, ALT, and AST in high NP treatment groups were increased compared with the control group.…”

Long noncoding RNA NEAT1 suppresses hepatocyte proliferation in fulminant hepatic failure through increased recruitment of EZH2 to the LATS2 promoter region and promotion of H3K27me3 methylation

“…FHF, accompanied by coagulopathy, hepatic encephalopathy, jaundice, and hydroperitoneum pathologies, is associated with high mortality rates due to the lack of effective therapies except for liver transplantation 2 . However, owing to the constant shortage of liver donors, complications, and high costs, liver transplantation is not a viable option for many patients 3 . It is therefore imperative to identify and develop novel therapeutic approaches to raise the quality of life of patients suffering from FHF.…”