目的观察栉孔扇贝裙边糖胺聚糖(SS-GAG)对体外培养的血管平滑肌细胞(VSMC)增殖的抑制作用及原癌基因(c-myc)mRNA表达的影响,并探讨SS-GAG抗动脉粥样硬化(AS)的作用机制。方法建立碱性成纤维细胞生长因子(bFGF)诱导的VSMC增殖模型,用MTT法观察bFGF、SS-GAG对VSMC增殖活性的影响;用原位杂交方法观察SS-GAG对bFGF诱导增殖的VSMC内c-myc mRNA表达的影响。结果bFGF模型组细胞活性最高,与正常对照组比较,差异有统计学意义,不同浓度的SS-GAG组细胞增殖活性均低于模型组细胞,差别有统计学意义;bFGF诱导增殖的VSMC内c-myc mRNA基因表达强度明显高于对照组;与模型组比较,SS-GAG作用后,增殖的VSMC内c-myc mRNA表达强度和阳性细胞数量均减少,差别有统计学意义。结论bFGF对VSMC有明显的促增殖作用,SS-GAG能显著抑制VSMC增殖,且对bFGF诱导增殖的VSMC的c-myc mRNA的阳性表达有抑制作用。
OBJECTIVE To observe the depressant effects of scallop skirts glyeosaminoglycan (SS-GAG) on the proliferation of vascular smooth muscle cells(VSMC) as well as on the expression of c-myc mRNA, and to explore the mechanism of SS-GAG in antiatherosclerosis. METHODS The cell proliferation model of VSMC induced by basic fibroblast growth factor (bFGF) was established. MTT chromatometry was applied to observe the effects of bFGF and SS-GAG on the proliferation of VSMC In situ hybridization was used to observe effects of SS-GAG on the mRNA expression of c-myc in proliferative VSMC induced by bFGF. RESULTS The cell activities in model group of bFGF was the highest. Its difference had statistical significance. Cell proliferation activities in different concentrations of SS-GAG groups were all lower than those of model group. The difference showed statistical significance. The gene expressions of c-myc mRNA VSMC group induced by bFGF were obviously higher than that of control group. Compared with the model group, the expression intensity and positive cells population were all reduced in proliferative VSMC affected by SS- GAG. CONCLUSION The bFGF shows evident effect on the promotion of VSMC proliferation while SS-GAG can inhibit the proliferation of VSMC notably and can depress the positive expression of c-myc of VSMC induced by bFGF.