Liver Fibrinolysis Particles Of Rat Liver Fibrosis And Liver Tissues Of ¦Á-sma And Pdgf Affect Experimental Research

Purposes and Objectives: To investigate the anti-hepatic fibrosis molecular mechanism of liver-fiber soluble grains (LFSG), thus providing a theory foundation for developing the traditional Chinese medicine on anti-hepatic fibrosis.Methods: The fibrosis rat model was induced by multiple factors of CCl₄ and ethanol, and was given the LFSGs which consisted of Chinese Drug, huangdi, danggui, sanqi, sangkanzi, guibanjiao, erjiao, and their effects on fibrosis rat model was studied. During the study, the general conditions, liver weight and body weights of each group rat, and pathology change of hepatic fibrosis by appling HE dye were observed. In addition, serology index was measured by immunity method and ELISA method, andα-SMA, PDGF-BB and liver PDGFR-ββmRNA expression of liver organ were detected by immunohistochemistry method and RT-PCR. These results were compared with those of the positive control group (PC).Results1 The general condition, liver weight, body weightCompared with normal group (N), liver weight and body weight of model group (M) all had an obvious difference (P<0.01), indicatiing that modeling was successful. After imposing medicine intervention, liver weights of various groups decreased, body weights increased, thus the ratio of two values decreased. This suggests that there was an obvious difference between the therapy groups (T) and model group other than the little difference between the high dosage group (HD) and group PC (P>0.05).2 The pathologic histology observationHepatic fibrosis gradually formed along with the increase of the CCL₄ injection number and time. The hepatic fibrosis degrees of groups T were less than that of group M (P<0.05), whereas in contrasted with group PC, middle dosage group (MD) and group HD did not have an obvious difference.3 The serum hepatic fibrosis indexIn comparison with those of group N, HA, LN, PCIII and IVC levels of groups T obviously increased and had a clear diversity. The four indexes of groups T were less than those of group M (P<0.01), especially for groups MD and HD. HA content was much higher than those of the rest three indexs.4 The measurement of IL-10 content1L-10 contents in the serum of various groups T increased and were obviously higher than that of group M, and thus there were an obvious difference between groups T and M. IL-10 contents increased with an increase in the dosage. However, groups MD and low dosage group (LD) did not vary much, and they obviously departed from groups HD andPC (P<0.05). Correspondingly, groups HD and PC did not have a marked difference (P>0.05), while they vary much from group N (P<0.05).5 The expression of the liverα-SMA contentThe liverα-SMA content was individually measured by immunohistochemistry and RT-PCR, and the results indicated that LFSG can obviously decrease theα-SMA content with the increase of dosage, groups MD and HD did not vary much from group PC (P>0.05), and theα-SMA content of groups T obviously reduced while there were marked differences between them and group M.6 The expression of liver PDGF—BB contentThe statistical results showed that LFSG can decrease the content of PDGF-BB which did not have an obvious difference from group PC (P>0.05), contrary to group M.7 The liver PDGFR-ββmRNA expressionDGFR-ββmRNA was determined by RT-PCR method. The results showed the value of group M was higher than that of groups T, and the increase of dosage can effectively lower the content of DGFR-ββmRNA.ConclusionsThough the occurrence mechanism of hepatic fibrosis is complicated, this study only discussed it from one aspect. The experimental results indicated PGDF was an important cell factor to accelerate hepatic fibrosis, andα-SMA was a symbol to activate HSC. PDGF-BB can combine with the receptors to induce a series of reactions, and eventually led to the formation of hepatic fibrosis. LFSGs can effectively improve the general conditions, liver weights, and body weights of the fibrosis rat induced by the multiple factors of CCl₄, and thus obviously changed the pathology of fibrosis rat and their biochemical indexs. The decrease of α-SMA, PDGF-BB, PDGFR-ββmRNA indicated that LFSGs may lower the translation level expression of PDGFR, and restrain the combination of PDGF and the receptor, which may be the anti- hepatic fibrosis occurance mechanism of LFSGs.