| ObjectiveTo explore the effects of octreotide （OCT） on expressions of Leptin and functionalleptin receptor （OB-Rb） of experimental liver fibrosis in rats. Thereby learn more aboutthe relationships between liver fibrosis and the expression of Leptin and its receptor,and observe the effects of OCT in liver fibrosis, and also look forward to opening theperspective on the study of OCT contributing to liver fibrosis, then provide sometheoretical basis for further experiments.Methods54adult male SD rats were randomly divided into three groups: normal group, liverfibrosis model group and the model rats which administered OCT. The liver fibrosismodels in rats were established by Carbon Tetrachloride with compound factors. OCTwith abdominal subcutaneous injection was administered twice a day in OCT group. Itcomes to6weeks. Three groups of rats were sacrificed randomly on the2,4,6weeksrespectively. The levels of serum total bilirubin （TBIL）, alanine aminotransferase （ALT）,aspartate aminotransferase （AST）, albumin （ALB） were tested, the concentration ofLeptin and transforming growth factor beta1（TGF-β1） of the rats was analysed by usingradio immune-assay, and the histopathology changes were observed by HE staining andVG staining; The immunohistochemical technique was used for detccting the leptin andOB-Rb protein expression. The results are expressed as the mean±S.D. Makesstatistics analysis processing using the SPSS17.0software, the data were compared bythe single factor variance analysis （one-way ANOVA）. Differences were examined using LSD-t analysis.Results1. Compared with normal group, the levels of serum TBIL, ALT, AST in model groupand OCT group went up significantly, the level of ALB went down （P<0.05）;Compared with model group, the levels of liver function improved significantly inthe4and6weeks （P<0.05）, but no significant difference in the2weeks betweenthe two groups, only the difference of ALT levels was statistically significant（P<0.05）.2. Using radioimmunoassay to test the serum Leptin and TGF-β1levels, statisticsshow: compared with normal group, the levels of serum Leptin of TGF-β1in modelgroup and OCT group went up sharply （P<0.05）; Compared with model group, thelevels of serum Leptin and TGF-β1in OCT group went down significantly（P<0.05）.3. Liver pathological changes: the liver specimens were observed under microscopeafter HE and VG staining, in the normal rats, the normal structure of the hepaticlobule and portal district, liver cells showed a cord-like distribution, no liver cellsnecrosis were observed; In the liver fibrosis model rats, destruction of hepatic cordsdisorganized, showing liver cells punctate necrosis, fatty degeneration andinfiltration of inflammatory cells, stromal hyperplasia, expansion of the portal area,a large number of fibrous septa form were observed, with the time goes by, the liverpathological changes were aggravated; While in the OCT group, there were lessdamaged in lobules of liver degeneration, liver cells necrosis and collage fibers, butthere were still incomplete pseudolobule formation in the very small number of ratliver tissue.4. IHC: Leptin have no expression in the normal liver tissue, only a minimumexpression in the portal area and hepatic cord stromal cells were found, and also OB-Rb have no expression in the normal liver tissue; In the fibrosis liver tissue, theexpression of Leptin and OB-Rb enhanced, Leptin express common in the HSC,positive material located in the cytoplasm. OB-Rb express in the non-parenchymalcells in the portal vein, lobular central vein, positive expression of material in thecytoplasm and cell membrane, little located in the nucleus. Statistics show that:compared with normal group, Leptin and OB-Rb expression was significantlyenhanced in model group and OCT group （P<0.05）, all the two protein expressionenhanced with time; Compared with model group, in the same time point, the twoprotein expression reduced in OCT group （P<0.05）.ConclusionOCT can ease the degree of hepatic function injury, delay the progress of liver fibrosis;OCT may inhibits the start of the early stage of liver fibrosis, reduces the levels ofserum Leptin and TGF-β1, and inhibits the expression of leptin in the liver tissue,prevents the combination between Leptin and OB-Rb, thereby inhibits the activationand proliferation of HSC, and play the pharmacological effects of anti-hepatic fibrosis. |
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