目的探究人参皂苷对小鼠晚期乳腺癌模型的抑瘤作用。方法小鼠适应性饲养1周后将4T1乳腺癌细胞悬液1 m L(1.0×1010L-1)接种于右胸部皮下建立晚期乳腺癌模型。30只BALB/c小鼠晚期乳腺癌模型随机分为模型组、环磷酰胺组、人参皂苷低...目的探究人参皂苷对小鼠晚期乳腺癌模型的抑瘤作用。方法小鼠适应性饲养1周后将4T1乳腺癌细胞悬液1 m L(1.0×1010L-1)接种于右胸部皮下建立晚期乳腺癌模型。30只BALB/c小鼠晚期乳腺癌模型随机分为模型组、环磷酰胺组、人参皂苷低剂量组、人参皂苷中剂量组和人参皂苷高剂量组,每组6只。环磷酰胺组小鼠给予环磷酰胺2 mg·kg-1,腹腔注射,隔日1次;人参皂苷低、中、高剂量组小鼠分别给予0.5、1.0、2.0 mg·kg-1的人参皂苷灌胃;模型组小鼠给予2 m L·kg-1的无菌生理盐水灌胃;灌胃均每日1次,连续4周。苏木精-伊红染色观察各组小鼠乳腺癌组织的病理改变,并比较各组小鼠的癌瘤质量、体积,抑瘤率,肺转移结节数及肿瘤转移抑制率。结果环磷酰胺组和人参皂苷低、中、高剂量组小鼠癌瘤质量和体积均显著小于模型组(P<0.05),抑瘤率显著高于模型组(P<0.05);人参皂苷中剂量组小鼠癌瘤质量、体积及抑瘤率与环磷酰胺组比较差异均无统计学意义(P>0.05);人参皂苷高剂量组小鼠癌瘤质量和体积均显著小于环磷酰胺组(P<0.05),抑瘤率显著高于环磷酰胺组(P<0.05);人参皂苷中、高剂量组小鼠癌瘤质量和体积均显著小于人参皂苷低剂量组(P<0.05),抑瘤率显著高于人参皂苷低剂量组(P<0.05);人参皂苷高剂量组小鼠癌瘤质量和体积均小于人参皂苷中剂量组,抑瘤率高于人参皂苷中剂量组,但差异均无统计学意义(P>0.05)。环磷酰胺组和人参皂苷低、中、高剂量组小鼠肺转移结节数显著少于模型组(P<0.05),肺转移抑制率显著高于模型组(P<0.05);人参皂苷中剂量组小鼠肺转移结节数及肺转移抑制率与环磷酰胺组比较差异均无统计学意义(P>0.05);人参皂苷高剂量组小鼠肺转移结节数显著少于环磷酰胺组(P<0.05),肺转移抑制率显著高于环磷酰胺组(P<0.05);人参皂苷中、高剂量组小鼠肺转移结节数显著少于展开更多
AIM: To explore effects of telomerase RNA-targeting phosphorothioate antisense oligodeoxynucleotides (PS-ASODN) on growth of human gastrointestinal stromal tumors transplanted in mice. METHODS: A SCID mouse model for ...AIM: To explore effects of telomerase RNA-targeting phosphorothioate antisense oligodeoxynucleotides (PS-ASODN) on growth of human gastrointestinal stromal tumors transplanted in mice. METHODS: A SCID mouse model for transplantation of human gastrointestinal stromal tumors (GISTs) was established using tumor cells from a patient who was diagnosed with GIST and consequently had been treated with imatinib. GIST cells cultured for 10 passages were used for inoculation into mice. Transfection of PS-ASODN was carried out with Lipotap Liposomal Transfection Reagent. GISTs that subsequently developed in SCID mice were subjected to intratumoral injection once daily from day 7 to day 28 postinoculation, and mice were divided into the following four groups according to treatment: PS-ASODN group (5.00 μmoL/L of oligonucleotide, each mouse received 0.2 mL once daily); imatinib group (0.1 mg/g body weight); liposome negative control group (0.01 mL/g); and saline group (0.01 mL/g). On day 28, the mice were sacrificed, and tumor attributes including weight and longest and shortest diameters were measured. Tumor growth was compared between treatment groups, and telomerase activity was measured by enzyme-linked immunosorbent assay. Apoptosis was examined by flow cytometry. Real-time polymerase chain reaction was used to detect expression of the mRNA encoding the apoptosis inhibition B-cell leukemia/lymphoma 2 (bcl-2 ) gene. RESULTS: In the PS-ASODN group, tumor growth was inhibited by 59.437%, which was markedly higher than in the imatinib group (11.071%) and liposome negative control group (2.759%) [tumor inhibition=(mean tumor weight of control group - mean tumor weight of treatment group)/(mean tumor weight of control group) × 100%]. Telomerase activity was significantly lower (P < 0.01) in the PS-ASODN group (0.689 ± 0.158) compared with the imatinib group (1.838 ± 0.241), liposome negative control group (2.013 ± 0.273), and saline group (2.004 ± 0.163). Flow cytometry revealed that the apoptosis rate of tumor cells tre展开更多
文摘目的探究人参皂苷对小鼠晚期乳腺癌模型的抑瘤作用。方法小鼠适应性饲养1周后将4T1乳腺癌细胞悬液1 m L(1.0×1010L-1)接种于右胸部皮下建立晚期乳腺癌模型。30只BALB/c小鼠晚期乳腺癌模型随机分为模型组、环磷酰胺组、人参皂苷低剂量组、人参皂苷中剂量组和人参皂苷高剂量组,每组6只。环磷酰胺组小鼠给予环磷酰胺2 mg·kg-1,腹腔注射,隔日1次;人参皂苷低、中、高剂量组小鼠分别给予0.5、1.0、2.0 mg·kg-1的人参皂苷灌胃;模型组小鼠给予2 m L·kg-1的无菌生理盐水灌胃;灌胃均每日1次,连续4周。苏木精-伊红染色观察各组小鼠乳腺癌组织的病理改变,并比较各组小鼠的癌瘤质量、体积,抑瘤率,肺转移结节数及肿瘤转移抑制率。结果环磷酰胺组和人参皂苷低、中、高剂量组小鼠癌瘤质量和体积均显著小于模型组(P<0.05),抑瘤率显著高于模型组(P<0.05);人参皂苷中剂量组小鼠癌瘤质量、体积及抑瘤率与环磷酰胺组比较差异均无统计学意义(P>0.05);人参皂苷高剂量组小鼠癌瘤质量和体积均显著小于环磷酰胺组(P<0.05),抑瘤率显著高于环磷酰胺组(P<0.05);人参皂苷中、高剂量组小鼠癌瘤质量和体积均显著小于人参皂苷低剂量组(P<0.05),抑瘤率显著高于人参皂苷低剂量组(P<0.05);人参皂苷高剂量组小鼠癌瘤质量和体积均小于人参皂苷中剂量组,抑瘤率高于人参皂苷中剂量组,但差异均无统计学意义(P>0.05)。环磷酰胺组和人参皂苷低、中、高剂量组小鼠肺转移结节数显著少于模型组(P<0.05),肺转移抑制率显著高于模型组(P<0.05);人参皂苷中剂量组小鼠肺转移结节数及肺转移抑制率与环磷酰胺组比较差异均无统计学意义(P>0.05);人参皂苷高剂量组小鼠肺转移结节数显著少于环磷酰胺组(P<0.05),肺转移抑制率显著高于环磷酰胺组(P<0.05);人参皂苷中、高剂量组小鼠肺转移结节数显著少于
基金Supported by The Natural Science Foundation of Zhejiang Province, No. Y201016273
文摘AIM: To explore effects of telomerase RNA-targeting phosphorothioate antisense oligodeoxynucleotides (PS-ASODN) on growth of human gastrointestinal stromal tumors transplanted in mice. METHODS: A SCID mouse model for transplantation of human gastrointestinal stromal tumors (GISTs) was established using tumor cells from a patient who was diagnosed with GIST and consequently had been treated with imatinib. GIST cells cultured for 10 passages were used for inoculation into mice. Transfection of PS-ASODN was carried out with Lipotap Liposomal Transfection Reagent. GISTs that subsequently developed in SCID mice were subjected to intratumoral injection once daily from day 7 to day 28 postinoculation, and mice were divided into the following four groups according to treatment: PS-ASODN group (5.00 μmoL/L of oligonucleotide, each mouse received 0.2 mL once daily); imatinib group (0.1 mg/g body weight); liposome negative control group (0.01 mL/g); and saline group (0.01 mL/g). On day 28, the mice were sacrificed, and tumor attributes including weight and longest and shortest diameters were measured. Tumor growth was compared between treatment groups, and telomerase activity was measured by enzyme-linked immunosorbent assay. Apoptosis was examined by flow cytometry. Real-time polymerase chain reaction was used to detect expression of the mRNA encoding the apoptosis inhibition B-cell leukemia/lymphoma 2 (bcl-2 ) gene. RESULTS: In the PS-ASODN group, tumor growth was inhibited by 59.437%, which was markedly higher than in the imatinib group (11.071%) and liposome negative control group (2.759%) [tumor inhibition=(mean tumor weight of control group - mean tumor weight of treatment group)/(mean tumor weight of control group) × 100%]. Telomerase activity was significantly lower (P < 0.01) in the PS-ASODN group (0.689 ± 0.158) compared with the imatinib group (1.838 ± 0.241), liposome negative control group (2.013 ± 0.273), and saline group (2.004 ± 0.163). Flow cytometry revealed that the apoptosis rate of tumor cells tre
