ABSTRACT
Objective To investigate the effect of bicyclol on liver tissue proliferation in mice with tetracycline-induced fatty liver. Methods Fifty ICR mice were randomly assigned into 5 groups (10 each): normal group (control), tetracycline 6h group, bicyclol 6h group, tetracycline 24h group and bicyclol 24h group. Mice in the two bicyclol groups received bicyclol (300mg/ kg) by gavage for 3 times in 12h interval, meanwhile, those in the other groups received the equal amount of forming agents. Tetracycline (200mg/kg) was then injected intraperitoneally to the mice in bicyclol groups and tetracycline groups 1h after the last dose of bicyclol, and mice in control group received equal amount and pH of saline. The liver issues and blood samples from eyes were collected 6h and 24h after tetracycline injection for detection of the corresponding indicators. RT-PCR was performed to detect the gene expression of proliferation index (PCNA, cyclin D1 and c-myc), Western blotting was performed to detect the expression of Cyclin D1 in liver tissue, and immunohistochemistry was employed to detect the expression of PCNA and c-myc proteins. Results The expression level of PCNA gene 6h after tetracycline injection in mice of tetracycline group was 43% of that in control group, meanwhile the expression of protein also reduced obviously. Bicyclol remarkably inhibited the decrease of PCNA gene and protein expressions at early time (6h) of fatty liver. In addition, the expression of cyclin D1 gene in tetracycline 24h group was 59%, and the expression of c-myc was 5.7 folds of that in control group. Bicyclol remarkably up-regulated the gene expressions of cyclin D1 and c-myc 6h after tetracycline injection, and up-regulated the protein expression of cyclin D1 24h after tetracycline injection. Conclusion Bicyclol can enhance hepatocyte proliferation of mice with tetracycline-induced fatty liver by up-regulation of PCNA, cyclin D1 and c-myc expression.
ABSTRACT
Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease. It covers a spectrum of liver diseases that range from hepatic steatosis to steatohepatitis and cirrhosis. The increase in its prevalence is linked to obesity and type 2 diabetes. More evidence shows a relation between overgrowth of gut microbiota with NAFLD and non-alcoholic steatohepatitis (NASH). Recently, many studies indicate that probiotics have very good effcts on improving NAFLD. Probiotics have been seen as a new way of treating NAFLD. But probiotics as treatment of NAFLD still need substantiation through more trials with a larger sample size and with longer-term clinical follow-up. Therefore, the research progress in probiotics treatment on animal experiments and clinical trials in NAFLD is reviewed in order to further understand the role of probiotics treatment, and provide the basis for the treatment of NAFLD.
ABSTRACT
The present study was performed to investigate the effect of bicyclol on hepatic microsomal cytochrome P450 (CYP) activity, as well as gene and protein expressions in rats after partial hepatectomy (PH). Bicyclol (300 mg x kg(-1)) was given to rats subjected to 70% hepatectomy three times before operation. At 6 and 48 h after PH, blood and liver tissue samples were collected for the measurement of serum alanine aminotransferase (ALT), hepatic microsomal malondialdehyde (MDA) and total hepatic CYP content. The activities of four CYP isozymes were detected with liquid chromatography-mass spectrometry (LC-MS) and the gene and protein expressions were determined by RT-PCR and Western blotting assay. As a result, bicyclol pretreatment markedly inhibited the elevation of serum ALT and hepatic microsomal MDA, and prevented the decrease of total hepatic CYP content in PH rats. In addition, bicyclol significantly attenuated the reduction of CYP2C6 activity and mRNA expression, as well as the reduction of CYP2C11 activity in PH rats. Bicyclol can inhibit the decrease of CYP3A1/2 activity, and up-regulate the mRNA and protein expressions of CYP3A1 and CYP2E1. These results showed that bicyclol pretreatment might ameliorate abnormality in CYP450 isoforms during liver regeneration after PH, and this protective effect was likely due to its anti-oxidative property and enzyme induction.