Combined detection of AFP-L3, GP73 and TIP30 enhances diagnostic accuracy for HBV-related cirrhosis and hepatocellular carcinoma.

OBJECTIVE: To investigate the value of combined tests of serum Golgi protein-73, alpha-fetoprotein- L3 and Tat-interacting protein-30 in the diagnosis of hepatitis B virus related cirrhosis and hepatocellular carcinoma. METHODS: The cross-sectional study was conducted at Yuebei People's Hospital, Guangdong, China, from January to October 2017, and comprised hepatitis B patients and healthy controls. Serum Golgi protein-73, alpha-fetoprotein-L3 and Tat-interacting protein-30 levels in both groups were detected by enzyme-linked immunosorbent assay (ELISA). Alpha-fetoprotein-L3 was separated and quantified by electrochemiluminescence immunoas says and the percentage of alpha-fetoprotein-L3 to alphafetoprotein was calculated. RESULTS: Of the 721 subjects, 525(%) were patients and 196(%) were healthy controls. Among the patients, 271(%) had chronic hepatitis B, 161(%) had liver cirrhosis and 93(%) had hepatocellular carcinoma. Serum Golgi protein-73, alpha-fetoprotein-L3 and Tat-interacting protein-30 levels were significantly different in the hepatocellular carcinoma patients compared to controls, and those with chronic hepatitis and liver cirrhosis (p<0.01 each). The sensitivity and specificity of the combined detection of the three serum levels for diagnosing cirrhosis were 78.26% and 86.72%. The corresponding values for diagnosing hepatocellular carcinoma were 86.02% and 92.51%. CONCLUSIONS: Combined detection of Golgi protein-73, alpha fetoprotein-L3 and Tat-interacting protein was found to have the potential to improve diagnostic accuracy.

Imidazoline I2 receptor inhibitor idazoxan regulates the progression of hepatic fibrosis via Akt-Nrf2-Smad2/3 signaling pathway.

Liver fibrosis is a global health problem and its relationship with imidazoline I2 receptor has not been reported. This study aimed to investigate the effects and underlying mechanisms of imidazoline I2 receptor (I2R) inhibitor idazoxan (IDA) on carbon tetrachloride (CCl4)-induced liver fibrosis. In vivo liver fibrosis in mice was induced by intraperitoneally injections of CCl4 for eight weeks, and in vitro studies were performed on activated LX2 cells treated with transforming growth factor-ß (TGF-ß). Our results showed that IDA significantly improved liver inflammation, ameliorated hepatic stellate cells activation and reduced collagen accumulation by suppressing the pro-fibrogenic signaling of TGF-ß/Smad. Further investigation showed that IDA significantly balanced oxidative stress through improving the expressions and activities of anti-oxidant and detoxifying enzymes and activating Nrf2-the key defender against oxidative stress with anti-fibrotic potentials. Even more impressively, knock out of Nrf2 or suppression of Akt by perifosine (PE) eliminated the anti-oxidant and anti-fibrotic effects of IDA in vivo and in vitro, suggesting that Akt/Nrf2 constitutes a critical component of IDA's protective functions. Taken together, IDA exhibits potent effects against liver fibrosis via Akt-Nrf2-Smad2/3 signaling pathway, which suggests that specifically targeting I2R may be a potentially useful therapeutic strategy for liver fibrosis.