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AIM:To study the anti-hapatofibrosis mechanism of Bie JiaJian oral liquid(BOL).METHODS:The model was induced by subcutaneousinjection of CCl_4.BOL was administered and the change ofserum hyaluronic acid(HA)and laminin(LN)was observedand the degeneration of liver cells and the degree of fibrehyperplasia analyzed.Changes of ultra micro-structure inliver cells were observed in some samples.RESULTS:HA was reduced in both the groupa with low andhigh dosage of BOL.which showed a remarkable differenceas compared with that of the model group(low dosagegroup:376.15μg/L±35.48μg/L vs 806.07μg/L±98.49μg/L,P<0.05;high dosage group:340.14μg/L±30.18μg/L vs806.07μg/L±98.49μg/L,P<0,05).The LN content of lowand high dosage group of BOL was lower than that of modelgroup(low dosage group:71.99μg/L±8.15μg/L vs 133.94μg/L±14.45μg/L,P<0.01;high dosage group:71.68μg/L±11.62μg/L vs 133.94μg/L±14.45μg/L,P<0.01)andcolchicine group(low dosage group:71.99μg/L±8.15μg/Lvs 118.28μg/L±16.13μg/L,P<0.05;high dosage group:71.68μg/L±11.62μg/L vs 118.28μg/L±16.13μg/L,P<0.05).Examined by Rldit,BOL could reduce thedegeneration and necrosis of liver cells(X~2=11.99P<0.05),the degree of fibre hyperplasia(X~2=13.24P<0.05)and the pathological change of ultra micro-structure as well.CONCLUSION:The BOL has certain therapeutic effect on theexperiment hepatoflbrosis.Its mechanisms might include:protecting the function of liver cells,inhibiting excessivesynthesis and ascretion of extracelluar matrix from hepaticatellete cells,relieving the capillarization of hepaticsinusold,Improving liver micro-clrculation,and regulatingimmune function.
AIM: To study the anti-hapatofibrosis mechanism of Bie JiaJian oral liquid (BOL) .METHODS: The model was induced by subcutaneous injection of CCl_4.BOL was administered and the change of serum hyaluronic acid (HA) and laminin (LN) was observed and the degeneration of liver cells and the degree of fib hyperplasia analyzed. Changes in ultra micro-structure inliver cells were observed in some samples .RESULTS: HA was reduced in both the groupa with low and high dosage of BOL.which showed a remarkable differenceas compared with that of the model group (low dosagegroup: 376.15μg / L ± 35.48μg / L vs 806.07μg / L ± 98.49μg / L, P <0.05; high dosage group: 340.14μg / L ± 30.18μg / L vs806.07μg / L ± 98.49 μg / L, P <0,05). The LN content of low and high dosage group of BOL was lower than that of model group (low dosage group: 71.99 μg / L ± 8.15 μg / L vs 133.94 μg / L ± 14.45 μg / L, P <0.01; high dosage group: 71.68μg / L ± 11.62μg / L vs 133.94μg / L ± 14.45μg / L, P <0.01) and colchicine group (low dosage group: 71.99μg / L ± 8.15μg / Lvs 118.28 μg / L ± 16.1 3μg / L, P <0.05; high dosage group: 71.68μg / L ± 11.62μg / L vs 118.28μg / L ± 16.13μg / L, P <0.05) .Excreted by Rldit, BOL could reduce the degeneration and necrosis of liver cells (X ~ 2 = 11.99P <0.05), the degree of fiber hyperplasia (X ~ 2 = 13.24P <0.05) and the pathological change of ultra micro-structure as well. CONCLUSION: The BOL has certain therapeutic effect on the experimental hepatoflbrosis. Its mechanisms might include: protecting the function of liver cells, inhibiting excessive synthesis and ascretion of extracelluar matrix from hepaticatellete cells, relieving the capillarization of hepatics in gold, Improving liver micro-clrculation, and regulatingimmune function.