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目的探讨三氧化二砷在体内对胰腺癌BXPC-3细胞移植瘤的抑制作用,并探讨其初步机制。方法建立胰腺癌裸鼠移植瘤模型,随机分为4组:模型组,低剂量、高剂量(2.5、5.0 mg/kg)三氧化二砷组和吉西他滨组,各组ip给药,作用2周后,检测实验前后裸鼠体质量变化,观察药物对肿瘤生长的影响,免疫组化检测肿瘤细胞增殖因子ki-67的表达,TUNEL法检测移植瘤组织的细胞凋亡。结果给药2周后,各组裸鼠体质量变化差异不显著,三氧化二砷和吉西他滨均可抑制裸鼠移植瘤的体积和质量,且三氧化二砷(5 mg/kg)组作用较强;免疫组化结果显示三氧化二砷可明显降低细胞增殖因子ki-67的阳性表达;TUNEL检测表明三氧化二砷可明显诱导移植瘤肿瘤细胞凋亡。结论三氧化二砷可抑制胰腺癌BXPC-3细胞在裸鼠体内的生长;作用机制可能为抑制肿瘤细胞增殖及促进肿瘤细胞凋亡。
Objective To investigate the inhibitory effect of arsenic trioxide on pancreatic cancer BXPC-3 cell xenografts in vivo and to explore its primary mechanism. Methods The model of pancreatic cancer xenografts in nude mice was established and randomly divided into 4 groups: model group, low dose and high dose (2.5, 5.0 mg / kg) arsenic trioxide group and gemcitabine group, each group ip administration, after 2 weeks, The changes of nude mice body mass before and after the experiment were observed. The effects of the drugs on the tumor growth were observed. The expression of the tumor cell proliferation factor ki-67 was detected by immunohistochemistry. The apoptosis of the tumor was detected by TUNEL. Results After 2 weeks of administration, there was no significant difference in body weight between groups. Both arsenic trioxide and gemcitabine inhibited the volume and quality of xenografts in nude mice, and the effect of arsenic trioxide (5 mg / kg) was stronger. The results of immunohistochemistry Arsenic trioxide was shown to significantly reduce the expression of cell proliferation factor ki-67; TUNEL assay showed that arsenic trioxide can obviously induce tumor cell apoptosis in xenografts. Conclusion Arsenic trioxide can inhibit the growth of pancreatic cancer BXPC-3 cells in nude mice. The mechanism may be to inhibit tumor cell proliferation and promote apoptosis of tumor cells.