The Study Of Drug-resistance Of Keloid Fibroblasts And The Inhibitory Effect Of Shi On Keloid Fibroblasts

Background: Keloid is regarded as a "benign",with characteristics of damaging the surrounding normal tissues,high rate of relapse after treatment and ability of drug resistance.Keloid is a human heir of pathological scar.Many studies reported in literature that keloid fibroblasts express a wide variety of tumor related factors,so that some scholars put forward “the hypothesis of keloid's tumor origin”.Domestic and foreign researchers found that SHI can inhibit cell proliferation,induce cell apoptosis,and inhibit inflammatory.SHI can inhibit the growth of a variety of malignant tumor cells.Because of the similarity of keloids and tumor in the biological characteristics,and the SHI could inhibit a wide variety of tumor cell growth and the effect of anti-inflammatory,we will study the keloid fibroblasts resistance and SHI on keloid fibroblasts growth impact.Methods: We gathered keloid fibroblasts from different body parts of different people,using flow cytometry analysis technology,to compare expression level of drug resistant protein of different site keloid fibroblasts.Various concentrations of SHI containing medium,and DMEM medium only were supplied to keloid fibroblasts,compare the treatment group and untreated group in cell proliferation,extracellular matrix formation and metabolism of differences.Results: The expression of ABCB1 protein in keloid's original generationin fibroblasts from chest is much more than other parts of the human body,and the difference is statistically significant.SHI preferentially inhibits cell proliferation,migration and induces apoptosis of keloid's fibroblasts in a time-and dose-dependent manner.Conclusion: Cells of high drug-resistant protein expression in keloid is likely to be cell sources of high drug-resistance and recurrence rate.Our results indicate that SHI preferentially inhibits cell proliferation,migration and induces apoptosis of fibroblasts in a time-and dose-dependent manner.In addition,we found that the proliferation-inhibiting and apoptosis-inducing abilities of SHI might be triggered via PI3k/AKT and NF-B/P53 signaling pathways.The data concluded from this study provides further evidence that supports the potential use of SHI as a novel keloid remediation therapy.