Abstract
This study investigated the expression and regulation of IL-6R in hepatitis B-associated moderate hepatic fibrosis and cirrhosis. Liver tissues, peripheral blood monocytes (PBMs) and serum were collected from 26 hepatitis B patients with liver fibrosis and 35 hepatitis B patients with liver cirrhosis. The levels of Il-6r mRNA expression in these samples were examined by quantitative real-time PCR and IL-6R protein levels were analyzed by western blot and ELISA. MiRNAs that regulate IL-6R expression were predicted by bioinformatics analysis, and validated by dual luciferase reporter assay. Compared with the hepatic fibrosis group, IL-6R was significantly upregulated at both mRNA and protein levels in liver tissues, PBMs and serum samples from the hepatic cirrhosis group (P<0.05). The 3′UTR of Il-6r mRNA was predicted to contain a miR-30b binding site and IL-6R was identified as a possible target of miR-30b. MiR-30b expression was significantly downregulated in samples from hepatic cirrhosis patients compared with hepatic fibrosis patients (P<0.05). In conclusion, IL-6R was upregulated while miR-30b was decreased in patients with liver cirrhosis. The miR-30 can directly regulate the expression of IL-6R.
Highlights
A prospective study showed that the annual incidence of cirrhosis developed from chronic hepatitis B is estimated to be 2.1% [1]
Il-6r mRNA expression was significantly increased in hepatic cirrhosis samples compared with hepatic fibrosis samples (Po0.05, Figure 1), suggesting that IL-6 receptor (IL-6R) is elevated in liver cirrhosis patients
IL-6R protein level was upregulated in patients with cirrhosis compared with patients with hepatic fibrosis (Po0.05, Figures 2 and 3), indicating that upregulated IL-6R expression may regulate the development of hepatic cirrhosis in hepatitis B patients
Summary
A prospective study showed that the annual incidence of cirrhosis developed from chronic hepatitis B is estimated to be 2.1% [1]. Another follow-up study on HBeAg negative chronic hepatitis B patients for an average of 9 years (varied from 1 to 18.4 years) showed that the incidence of cirrhosis transition is 23% [1,2,3]. Hepatic fibrosis may develop to cirrhosis [5], affecting the health and life of the patient greatly. It is highly important for the clinical treatment of hepatitis B to study the mechanism of transition from hepatic fibrosis to cirrhosis at the molecular level. The control of IL-6R in hepatitis B-associated liver fibrosis and cirrhosis and the regulatory pathway of IL-6R in this process has yet to be fully understood
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