论文部分内容阅读
AIM:To examine the expressions of matrix metalloprotein-ases-2(MMP-2)and tissue inhibitor of metalloproteinases-1(TIMP-1)in rat fibrotic liver and in normal rat hepatic stellatecells,and to investigate the changes in their expressionsin response to treatment with interleukin-10(IL-10)andplatelet-derived growth factor(PDGF).METHODS:Rat models of CCI_4-induced hepatic fibrosiswere established and the liver tissues were sampled fromthe rats with or without IL-10 treatment,and also from thecontrol rats.The expressions of MMP-2 and TIMP-1 in livertissues were detected by S-P immunohistochemistry,andtheir expression intensities were evaluated in differentgroups.Hepatic stellate cells(HSCs)were isolated fromnormal rat and cultured in vitro prior to exposure to PDGFtreatment or co-treatment with IL-10 and PDGF.MMP-2and TIMP-1 levels were measured by semi-quantitativereverse transcriptional polymerase chain reaction(RT-PCR).RESULTS:CCI_4-induced rat hepatic fibrosis models weresuccessfully established.The positive expressions of NMP-2and TIMP-1 increased obviously with the development ofhepatic fibrosis,especially in untreated model group(84.0%and 92.0%,P<0.01).The positive signals decreasedsignificantly following IL-10 treatment(39.3% and 71.4%,P<0.01 and P<0.05)in a time-dependent manner.TIMP-1mRNA in PDGF-treated group was significantly increasedtime-dependently in comparison with that of the controlgroup,but PDGF did not obviously affect MMP-2 expression.No difference was noted in TIMP-1 and MMP-2 expressionsin HSCs after IL-10 and PDGF treatment(P>0.05).CONCLUSION:MMP-2 and TIMP-1 expressions increasein liver tissues with the development of fibrosis,which canbe inhibited by exogenous IL-10 inhibitor.PDGF inducesthe up-regulation of TIMP-1 but not MMP-2 in the HSCs.IL-10 inhibits TIMP-1 and MMP-2 expressions in HSCsinduced by PDGF.
AIM: To examine the expressions of matrix metalloprotein-ases-2 (MMP-2) and tissue inhibitor of metalloproteinases-1 (TIMP-1) in rat fibrotic liver and in normal rat hepatic stellate cells, and to investigate the changes in their expressions in response to treatment with interleukin-10 (IL-10) and platelet-derived growth factor (PDGF). METHODS: Rat models of CCI_4-induced hepatic fibrosis established and the liver tissues were sampled from the rats with or without IL-10 treatment, and also from thecontrol rats. The expressions of MMP-2 and TIMP-1 in livertissues were detected by SP immunohistochemistry, andtheir expression intensities were evaluated in differentgroups.Hepatic stellate cells (HSCs) were isolated fromnormal rat and cultured in vitro prior to exposure to PDGFtreatment or co -treatment with IL-10 and PDGF. MMP-2 and TIMP-1 levels were measured by semi-quantitative reverse transcriptional polymerase chain reaction (RT-PCR) .RESULTS: CCI_4-induced rat hepatic fibrosis models weresuccessfully esta blished. The positive expressions of NMP-2 and TIMP-1 increased obviously with the development of hepatic fibrosis, especially in untreated model group (84.0% and 92.0%, P <0.01). The positive signals decreased solely ignited IL- 10 treatment 71.4%, P <0.01 and P <0.05 respectively) in a time-dependent manner. TMP-1 mRNA in PDGF-treated group was significantly increased-dependently in comparison with that of the control group, but PDGF did not have affect affect MMP-2 expression. No difference was noted in TIMP-1 and MMP-2 expressions in HSCs after IL-10 and PDGF treatment (P> 0.05) .CONCLUSION: MMP-2 and TIMP-1 expressions increasein liver tissues with the development of fibrosis, which can be inhibited by exogenous IL-10 inhibitor. PDGF induces up-regulation of TIMP-1 but not MMP-2 in the HSCs.IL-10 inhibits TIMP-1 and MMP-2 expressions in HSCs induced by PDGF.