参芪抑瘤方药物血清对胃癌MGC-803细胞增殖的影响

Effects of Medicinal Serum of Shenqi Yiliu Formula on Proliferation of Gastric Cancer MGC-803 Cells

目的观察参芪抑瘤方药物血清对胃癌MGC-803细胞增殖的影响,探讨其相关机制。方法以参芪抑瘤方不同浓度药物血清干预胃癌MGC-803细胞后,MTT法检测细胞增殖,流式细胞仪检测细胞周期,q RT-PCR检测CDKN1B、CDKN1C基因表达,Western blot检测p27、p57蛋白表达。结果 3%、5%、10%药物血清作用于MGC-803细胞24、48、72 h,细胞增殖水平显著降低(P<0.01),且与时间和剂量呈依赖关系;3%、5%、10%药物血清作用于MGC-803细胞24 h后,G0/G1期细胞增多,S期细胞减少;q RT-PCR检测结果显示,与对照组和空白血清组比较,药物血清各剂量组MGC-803细胞CDKN1B、CDKN1C m RNA表达显著上调(P<0.01);Western blot检测结果显示,与对照组比较,药物血清各剂量组MGC-803细胞p27、p57蛋白表达显著上调(P<0.01)。结论参芪抑瘤方药物血清可抑制胃癌MGC-803细胞的增殖,其机制可能是通过调节CDKN1B、CDKN1C m RNA和蛋白表达,进而干预细胞周期。

Objective To investigate the inhibitory effects of medicinal serum of Shenqi Yiliu Formula on cellproliferation of gastric cancer MGC-803cells;To discuss relevant mechanism.Methods After treated with differentconcentrations of medicinal serum of Shenqi Yiliu Formula,gastric cancer MGC-803cells were tested by thefollowing methods:MTT was employed to test the proliferation of gastric cancer MGC-803cells;Flow cytometrywas used to detect cell cycle;qRT-PCR was used to detect the genetic expressions of CDKN1B and CDKN1C;Western blot was employed to test the protein expressions of p27and p57.Results When3%,5%and10%medicinalserum of Shenqi Yiliu Formula was treated to MGC-803cells for24h,48h and72h,proliferation of cells decreasedsignificantly(P<0.01),with time-and dosage-dependent relationship.When3%,5%and10%medicinal serum ofShenqi Yiliu Formula was treated to MGC-803cells for24h,cells in G0/G1increased,decreased in S.qRT-PCRresults showed that compared with the blank control group and the negative control group,mRNA expressions ofCDKN1B and CDKN1C of MGC-803cells in medicinal serum all dose group increased significantly(P<0.01).Western blot results showed that compared with the blank control group,protein expressions of p27and p57ofMGC-803cells in medicinal serum all dose group increased significantly(P<0.01).Conclusion Medicinal serum ofShenqi Yiliu Formula can inhibit MGC-803cells proliferation and the mechanism may be through adjusting CDKN1B,CDKN1C mRNA and proteins expression to intervene in the cell cycle.