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AIM:To investigate the effect of Kangxian ruangan keli (KXR)on hepatic stellate cell (HSC) proliferation mediated byplatelet-derived growth factor (PDGF) and the underlyingmechanism.METHODS:In a serum-free culture system,HSCs weretreated with a KXR preparation for 24 hours,followed bystimulation with PDGF-BB for 24 hours.Then the cells wereincubated again in the medium containing KXR for 3 hoursstimulated with PDGF-BB for 5 minutes,and collected.Theproliferation of HSC was examined using an MTT assayand flow cytometry.Tyrosine phosphorylation was detectedwith Western blotting and visualized by the enhencedchemiluminescent (ECL) method.RESULTS:The OD values for the HSCs growing in the mediawithout and with addition of PDGF were 0.17±0.06 and0.82±0.05,respectively.The PDGF-induced increase washindered remarkably by KXR preparation in a dose-dependent manner.The reaction values for the systems with5 mg/mL,2.5 mg/mL and 1.25 mg/mL of KXR were 0.28±0.03,0.37±0.02 and 0.43±0.04,respectively.Moreover,thepercentages of S-phase cells in these KXR-containing culturesystems were 10.95±1.35,32.76±1.07 and 43.19±1.09,respectively,all of which were significantly lower than thatin the culture free of KXR (68.24±2.72).In addition,thevalues for tyrosine-phosphorylated protein in HSCs treatedwith 5 mg/mL and 1.25 mg/mL of KXR were 0.1349±0.0072and 0.1658±0.0025,respectively,which were smaller thanthat in the cells treated only with PDGF-BB (0.1813±0.0117).CONCLUSION:Within the dose range used in the presentstudy,KXR preparation shows an inhibitory effect on HSCproliferation induced by PDGF.The mechanism of this processmay involve interference with tyrosine phosphorylationmediated by PDGF.
AIM: To investigate the effect of Kangxian ruangan keli (KXR) on hepatic stellate cell (HSC) proliferation mediated by platelet-derived growth factor (PDGF) and the underlying mechanism. METHODS: In a serum-free culture system, HSCs were treated with a KXR preparation for 24 hours, followed bystimulation with PDGF-BB for 24 hours. The the cells wereincubated again in the medium containing KXR for 3 hoursstimulated with PDGF-BB for 5 minutes, and collected. The assay was performed using an MTT assay and flow cytometry. The PD values for the HSCs growing in the media with and without PDGF were 0.17 ± 0.06 and 0.82 ± 0.05, respectively. The PDGF-induced increase washindered remarkably by KXR preparation in a dose-dependent manner. The reaction values for the systems with 5 mg / mL, 2.5 mg / mL and 1.25 mg / mL of KXR were 0.28 ± 0.03, 0.37 ± 0.02 and 0.43 ± 0.04, respecti vely. Moreover, the per centages of S-phase cells in these KXR-containing cultures were 10.95 ± 1.35, 32.76 ± 1.07 and 43.19 ± 1.09, respectively, all of which were significantly lower than that of the culture of KXR (68.24 ± 2.72). In addition, thevalues for tyrosine-phosphorylated protein in HSCs treated with 5 mg / mL and 1.25 mg / mL of KXR were 0.1349 ± 0.0072 and 0.1658 ± 0.0025, respectively, which were smaller thanthat in the cells treated only with PDGF-BB (0.1813 ± 0.0117) .CONCLUSION: Within the dose range used in the present study, KXR preparation shows an inhibitory effect on HSC proteoliferation induced by PDGF. The mechanism of this processmay involve interference with tyrosine phosphorylationlated by PDGF.