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AIM To investigate the mechanisms ofsalvianolic acid A(SA-A)against liver fibrosisin vitro.METHODS NIH/3T3 fibroblasts were culturedroutinely,and incubated with 10~(-4)mol/L-10~(-7)mol/L SA-A for 22 h.The cell viability wasassayed by[~3H]proline incorporation,cellproliferation by[~3H]TdR incorporation,cellcollagen synthetic rate was measured with[~3H]proline impulse and collagenase digestionmethod.The total RNA was prepared from thecontrol cells and the drug treated cellsrespectively,and α(1)I pro-collagen mRNAexpression was semi-quantitatively analyzedwith RT-PCR.RESULTS 10~(-4)mol/L SA-A decreased cellviability and exerted some cytotoxiciy,while10~(-5)mol/L-10~(-7)mol/L SA-A did not affect cellviability,but inhibited cell proliferationsignificantly,and 10~(-6)mol/L SA-A had the besteffect on cell viability among theseconcentrations of drugs.10~(-5)mol/L-10~(-6)mol/LSA-A inhibited intracellular collagen syntheticrate,but no significant influence on extracellularcollagen secretion.Both 10~(-5)mol/L and10~(-6)mol/L SA-A could decrease α(1)I pro-collagen mRNA expression remarkably.CONCLUSION SA-A had potent action againstliver fibrosis.It inhibited NIH/3T3 fibroblastproliferation,intracellular collagen syntheticrate and type I pro-collagen gene expression,which may be one of the main mechanisms of thedrug.
AIM To investigate the mechanisms ofsalvianolic acid A(SA-A)against liver fibrosisin vitro.METHODS NIH/3T3 fibroblasts were culturedroutinely, and incubated with 10~(-4)mol/L-10~(-7)mol/L SA- A for 22 h.The cell viability wasassayed by[~3H]proline incorporation,cellproliferation by[~3H]TdR incorporation,cellcollagen synthetic rate was measured with[~3H]proline impulse and collagenase digestionmethod.The total RNA was prepared from thecontrol cells And the drug treated cellsrespectively,and α(1)I pro-collagen mRNA expression was semi-quantitatively analyzedwith RT-PCR.RESULTS 10~(-4)mol/L SA-A decreased cell viability and exerted some cytotoxiciy, while10~(-5 )mol/L-10~(-7)mol/L SA-A did not affect cell viability, but inhibited cell proliferationsignificantly,and 10~(-6)mol/L SA-A had the besteffect on cell viability among these concentrations of drugs .10~(-5)mol/L-10~(-6)mol/LSA-A inhibited intracellular collagen syntheticrate,but no significant influence on extracellularcollagen secretion.Bot h 10~(-5)mol/L and10~(-6)mol/L SA-A could decrease α(1)I pro-collagen mRNA expression remarkably.CONCLUSION SA-A had potent action against liver fibrosis.It inhibited NIH/ 3T3 fibroblastproliferation, intracellular collagen syntheticrate and type I pro-collagen gene expression,which may be one of the main mechanisms of the drug.