大黄素对SV－40转基因小鼠系膜细胞生长和c－mycmRNA表达的影响

Emodin inhibited SV-40 transgenic inesan-gial cell proliferation and C-myc mRNA ex-pression

利用从ＳＶ－４０病毒转基因小鼠肾脏分离得到的系膜细胞株（ＳＶ－４０ＭＣ），观察了大黄素对ＳＶ－４０和ＭＣ生长、增殖细胞核抗原（ＰＣＮＡ）及原癌基因ｃ－ｍｙｃｍＲＮＡ表达的影响，大黄素可明显抑制ＳＶ－４０ＭＣ３Ｈ－ＴｄＲ掺入且与剂量呈正相关。经大黄素（５μｇ／ｍｌ）作用的ＳＶ－４０ＭＣ，ＰＣＮＡ阴性细胞数明显高于对照（２８％ｖｓ。５．５％、ｐ＜０．００１）大黄素同样抑制ＳＶ－４０ＭＣ，ｃ－ｍｙｃｍＲＮＡ表达，且不受蛋白合成抑制剂放线菌酮的影响。结果表明：大黄素对异常增殖状态的系膜细胞生长也有明确抑制作用，细胞分裂周期受抑制、此过程与细胞周期基因ｃ－ｍｙｃ表达受抑有关。

Mesangial cells isolated from the kid-ney of sivia virus-40 transgenic mice (SV-40MC) had enhanced proliferative capacityand were responsible for the development ofprogressive glomerulosclerosis of the mice.In this paper'we investigated the effect ofEmodin on cell prolifertion , proliferative cellneclear antigen (PCNA) and C-myc mRNAexpression of SV-40MC. PCNA was detect-ed by four-layer PAP rnethod , C-myc mR-NA level by standard dot-blotting. 3H-TdRincorporation into SV-40MC was markedlyinhibited by Emodin in a dose-dependentnfianner. The arnount of H-TdR incorpora-tion at the dose 5 mg/L was 50% that ofcontrol. PCAN negative cells in Emodin (5mg/L ) treated SV-40MCs were 28%,wherase 5. 5% in control (P<0. 001 ) , andserurn-free cultured SV-40MC had low levelexpression of C-myc mRNA, but rnuchhigher level was detected in 5% FCS con-taining medium cultured cells. Interestingly,this over C-myc mRNA expression wasgreatly suppressed by Emodin (5mg/L).Cycloheximide, a protein synthesis in-hibitor,had no effects on this process. Con-clusion: Emodin inhibited the proliferationand cell cycle processes of SV-40MC. Theinhibition of Emotlin on the abnorrnal prolif-erative MC could be useful in treatment ofglomoru loscleros is .