Abstract
目的 探讨鹿茸多肽(PAP)促进软骨细胞增殖的机制.方法 以12.5、25.0、50.0、100.0 μg/mL不同浓度的PAP刺激软骨细胞,倒置相差显微镜观察软骨细胞生长情况,噻唑兰法(MTT)检测软骨细胞的生长增殖能力;以6、12、24、48 μg/mL不同浓度酪氨酸受体激酶阻断剂Genistein作用于受PAP刺激的软骨细胞,用MTT和流式细胞仪观察Genistein对PAP作用的影响;免疫组化SABC法检测核增殖抗原cyclinA在PAP和PAP+Genistein作用下的表达变化,RT-PCR法检测c-fos mRNA表达.结果 PAP作用下c-fos mRNA与cyclinA表达增加,S期的细胞比例增高,从6.4%增加到35.2%;Genistein作用后PAP的促增殖作用受到明显的抑制,S期的细胞降到4%,c-fos mRNA与cyclinA表达亦减少;单纯用Genistein不影响软骨细胞生长.结论 PAP可能通过酪氨酸受体蛋白激酶介导,作用下游的信号,引发立早基因c-fos表达,促进cyclinA的表达,引起更多的细胞进入有丝分裂期,从而促进软骨细胞增殖。
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