The relationship between the serum biochemical markers and hepatic fibrosis were analyzed. Results:The level of some serum biochemical markers Alb,Glo,HA,PCⅢ,CⅣ were correlated with the hepatic fibrosis stage,and the correlation coefficient(r) were-0.299,0.282,0.595,0.387,and 0.480 respectively.
Serum CIV、PCⅢ and HA were found to be closely related to the degree of fibrosis in 6 9 patients' liver biopsy studies,but no correlation could be found between these 3 markers,The sensitivity of CIV,PCⅢ,HA in detecting liver fibrosis were 73.9%,67.4%,67.4%with specificity of 95.7%, 9l.
And the degree of fibrosis was correlated with the activity of inflammation. Furthermore, with the increase in the degree of liver fibrosis, the level of serum AST, ALT, HA, liver tissue homogenate HyP, and the number of α-SMA positive HSC were increased.
Results HA and collegan Ⅳ were increased with the aggravation of fibrotic degree,and the difference between S4 and S1 S3 groups was significant. The cut off value of HA and collagen Ⅳ by ROC analysis had the sensitivity and specificity of 70%-80% in diagnosing liver cirrhosis.
MethodsWe transfered retrovirus-mediated antisense Smad 4cDNA into the CCl4/ethanol induced cirrhotic liver of Kunming mouse model to investigate the antisense-Smad 4 gene integration by Southern blot. The expression of Smad 4 in cirrhotic liver was observed by Northern blot, RT-PCR, and Western blot. The fibrotic degree of the livers among the three groups were compared.
In the non-treated cirrhotic liver, the expression of Smad 4 mRNA was significantly increased than normal liver, the antisense Smad 4 gene could decrease the expression of Smad 4. Compared with the non-treated liver, the fibrotic septa of the liver in the retrovirus-treated mouse were fewer,narrow, and incomplete,and their fibrotic degree of the treated-liver was reduced.
Hepatic steatosis, lobular inflammation, hepatocytic ballooning and fibrosis were presented widespread in NAFLD liver tissues.
Mild perisinusoidal fibrosis and periportal fibrosis were often observed in stage 1 cases.
According to the statistic analysis, hepatic steatosis was positively correlated with lobular inflammation, hepatocytic ballooning and fibrosis (r = 0.587, 0.488, 0.374, respectively, all P value >amp;lt; 0.01).
The number of microgranulomas, lipogranulomas and apoptotic bodies increased following severity of steatosis, lobular inflammation and fibrosis.
We suggest that the role of portal inflammation should be emphasized besides hepatic steatosis, lobular inflammation, hepatocyte ballooning and fibrosis in diagnosis and evaluation of NAFLD.