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厚壳贻贝提取物海生素(HSS)可抑制耐药 K562/ADM 肿瘤中 mdr1、BCR/ABL 和 sorcin 的表达。

Tegillarca granosa extract Haishengsu (HSS) suppresses expression of mdr1, BCR/ABL and sorcin in drug-resistant K562/ADM tumors in mice.

机构信息

Department of Hematology, Qilu Hospital of Shandong University, Jinan, Shangdong, PR China

出版信息

Adv Med Sci. 2013;58(1):112-7. doi: 10.2478/v10039-012-0069-8.

DOI:10.2478/v10039-012-0069-8
PMID:23729583
Abstract

PURPOSE

To evaluate the effect of Haishengsu (HSS), a protein extract from Tegillarca granosa, on multidrug-resistance genes mdr1, BCR/ABL and sorcin in transplanted tumors.

MATERIAL/METHODS: Mice were inoculated subcutaneously with a drug resistant leukemia cell line K562/ADM. Tumor-bearing animals were divided into control, adriamycin, HSS and combination therapy (adriamycin plus HSS) groups. Flow cytometry was used to detect apoptosis of tumor cells, and RT-PCR was used to evaluate the expression of mdr1, BCR/ABL and sorcin.

RESULTS

The apoptosis rate in the high (71.8%), medium (72.3%) and low doses HSS group (72.4%) was higher than in control (1.2%, p<0.01), adriamycin (34.4%, p<0.05) or combination therapy group (46.4%, p<0.05). The mean optical density of mdr1, BCR/ABL and sorcin in HSS groups was lower than in control, adriamycin and combination therapy group (p<0.01). The optical density of the three genes in high HSS group was lower than in medium and low HSS group (p<0.01).

CONCLUSIONS

Haishengsu promotes apoptosis of drug-resistant K562/ADM tumors in mice in a dose-dependent manner. The pro-apoptotic effect of Haishengsu may be related to a reduced expression of multidrug-resistance genes mdr1, BCR/ABL and sorcin.

摘要

目的

评价海生素(HS)——一种来自中国毛蚶的蛋白提取物对多药耐药基因 mdr1、BCR/ABL 和 sorcin 在移植瘤中的作用。

材料/方法:将耐药白血病细胞系 K562/ADM 皮下接种于小鼠,荷瘤动物分为对照组、阿霉素组、HS 组和联合治疗(阿霉素加 HS)组。采用流式细胞术检测肿瘤细胞凋亡,RT-PCR 法检测 mdr1、BCR/ABL 和 sorcin 的表达。

结果

HS 高、中、低剂量组(71.8%、72.3%和 72.4%)的凋亡率均高于对照组(1.2%,p<0.01)、阿霉素组(34.4%,p<0.05)或联合治疗组(46.4%,p<0.05)。HS 组 mdr1、BCR/ABL 和 sorcin 的平均光密度均低于对照组、阿霉素组和联合治疗组(p<0.01)。HS 高剂量组的三个基因的光密度均低于中、低剂量组(p<0.01)。

结论

海生素可呈剂量依赖性促进耐药 K562/ADM 肿瘤在小鼠体内的凋亡。海生素的促凋亡作用可能与多药耐药基因 mdr1、BCR/ABL 和 sorcin 的表达降低有关。

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