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Background and Purpose HBV infection is a serious public health problem. The world's approximately 350 million people with chronic HBV infection, about 100 million people a year die from HBV infection due to liver failure, cirrhosis, and primary liver cancer. In recent years, the incidence of fatty liver disease has increased year by year, has become the second largest in China and the Asia-Pacific region after the CHB liver disease. Fatty liver can induce the generation of extracellular matrix, resulting in the occurrence of fatty liver fibrosis and cirrhosis. Reported in the literature, 27% -51% of CHB patients with fatty liver, higher than the general population, the incidence of fatty liver. Therefore, HBV is involved in the development of fatty liver, liver disease research in the field has become a hot spot. This study was to explore the relationship and the possible mechanism of HBx protein and fatty liver from two levels of clinical and basic. Method 1 of the 18 patients with pathologically confirmed CHB hospitalized patients and 18 cases of CHB with fatty liver gender, age, blood lipids, fasting glucose, liver function, serum virological indicators; 2, immunohistochemical observation of liver tissue HBsAg HBcAg, HBx, LXRα and FAS protein expression. Image-Pro Plus5.0 software quantitative determination of HBsAg, HBcAg, HBx, LXRα and FAS protein mean optical density (mean density) value. The MTT colorimetric screening of sodium oleate optimal concentration and duration of action. Oil Red O staining HepG2.2.15 and HepG2 cells the degree of steatosis; determination of intracellular triglyceride content; Western blot detection of HBx, LXRα and FAS protein expression. Results 1 CHB and CHB patients with fatty liver disease cases in gender (P gt; 0.05), age (P gt; 0.05), TG (P gt; 0.05), CHOL (P gt; 0.05), ALT (121.75 ± 115.33vs 123.49 ± 102.57, P gt; 0.05), AST (63.51 ± 32.85vs57.17 ± 37.46, P gt; 0.05), fasting glucose (vs5.50 5.30 ± 0.40 ± 0.35, P gt; 0.05), HBsAg positive rate (100% vs100%, P gt; 0.05), the HBsAb positive rate (0 vs 0, P gt; 0.05), HBeAg positive rate (38.89% vs27.78%, P gt; 0.05) anti HBeAb positive rate (55.56% vs55.56% , P gt; 0.05), HBcAb positive rate (100% vs100%, P gt; 0.05), HBV-DNA load (1.52 * 107 + 2.45 * 107vs1.71 * 107 ± 1.62 * 107, P gt; 0.05) each the indexes no significant differences; constitute more than two sets of liver inflammation grade and fibrosis stage was no significant difference (P gt; 0.05); 18 patients with CHB patients with fatty liver disease patients, the degree of hepatic steatosis to light - the degree of steatosis mainly with chronic hepatitis inflammation grades (P gt; 0.05) and fibrosis stage (P gt; 0.05) has nothing to do. 2 immunohistochemistry results showed that HBsAg expressed in the cytoplasm of hepatocytes, HBcAg expression in the liver cell nuclei. CHB patients with fatty liver group and CHB group HBsAg and HBcAg expression positive rate of 100%, P gt; 0.05, the difference was not statistically significant. (T = 1.50, P gt; 0.05), HBcAg (t = 0.95, P gt; 0.05) the expression of strength, there was no significant difference in the two groups HBsAg. Of HBx (77.78% vs 83.33%), LXRα (77.78% vs 88.89%), FAS (83.33% vs 88.89%) of positive expression rate between CHB and CHB patients with fatty liver group no statistical difference (P gt; 0.05) . Of HBx (0.19 ± 0.08 vs 0.25 ± 0.09), of LXRα (0.16 ± 0.01 vs 0.21 ± 0.03), FAS expression strength (0.17 ± 0.02 vs 0.26 ± 0.07) in CHB patients with fatty liver group was significantly higher than the CHB group (P lt ; 0.05), and HBx in CHB patients with fatty liver group expression intensity in the cytoplasm and nucleus of CHB group were significantly higher than P lt; 0.05; correlation test analysis showed that HBsAg and of LXRα FAS (r = 0.33, r = 0.37, P gt; 0.05) and HBcAg of LXRα and FAS (r = 0.35, r = 0.26, P gt; 0.05) expression was not correlated. HBx and of LXRα FAS (r = 0.76, 0.68, P lt; 0.05) were positively correlated. The 3 of HepG2.2.15 and HepG2 cells steatosis modeling. 1) According to the results of MTT, sodium oleate induced concentration 40μg/ml, the best role period of 24h, 48h and 72h. 2) Oil Red O staining: in not refueling sodium handling the case, the period of HepG2.2.15 cells and HepG2 cells only see a very small amount of orange-red lipid droplets, lipid droplets HepG2.2.15 cells than HepG2 cells. After treatment of the sodium oleate, the lipid droplets within the cells in each group as the treatment time increased gradually, and have different degrees of integration. HepG2.2.15 cells in each group, however, lipid droplets were significantly more than the HepG2 cell group. 3) TG Determination: HepG2.2.15 cells was higher TG content than HepG2 cells (P lt; 0.05) in the case of not refueling sodium handling. The sodium oleate treatment, the TG content of HepG2.2.15 cells and HepG2 cells showed a time-dependent increase, The HepG2.2.15 cells 24,48,72 h TG content than those in the same time period HepG2 increase (P lt; 0.05) The difference was statistically significant. HBx protein expression: HBx protein in HepG2.2.15 cells express negative expression in HepG2 cells, P lt; 0.05, the difference was statistically significant. 5 of LXRα and FAS protein expression: the untreated group HepG2.2.15LXRα and FAS protein expression was significantly higher than in HepG2 cells group (P lt; 0.05). The sodium oleate treatment, the HepG2.2.15 cells LXRα and FAS protein in 24h, 48h, 72h than HepG2 cells the expression of the same time period increased significantly (P lt; 0.05), the difference was statistically significant. Conclusion HBx may in turn lead to induction of LXRα the FAS expression raised to participate in the the CHB merger fatty liver occurred.
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