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目的:观察大黄素对白血病K562细胞BALB/c裸鼠皮下移植瘤的抑制作用,检测肿瘤组织中Bax和Bcl-2的表达水平,探讨其作用机制。方法:建立裸鼠K562细胞皮下移植瘤模型,腹腔连续给药12d,处死裸鼠,称取瘤体质量,计算抑瘤率。采用HE染色光镜和透射电镜方法观察肿瘤细胞的凋亡情况,免疫组化方法观察肿瘤组织中Bax和Bcl-2蛋白表达情况,应用RT-PCR检测肿瘤组织中Bax和Bcl-2的mRNA水平。结果:各用药组抑瘤作用与阴性对照组相比差异均具有显著性(P<0.05),高浓度组与羟基脲组具有同等的抑瘤效应(P>0.05),光镜和电镜检测发现大黄素低、中、高浓度组均可见瘤细胞凋亡和坏死,其中以高浓度处理组最为显著,羟基脲处理组部分瘤细胞以坏死为主。免疫组化和RT-PCR结果表明大黄素处理后肿瘤组织中Bax蛋白和Bax mRNA表达上调,Bcl-2蛋白和Bcl-2mRNA表达下调。结论:大黄素可以明显抑制K562细胞在裸鼠体内的生长,其作用机制可能是通过调控肿瘤中Bax及Bcl-2的表达,从而促进细胞凋亡。
OBJECTIVE: To observe the inhibitory effect of emodin on leukemia K562 cells subcutaneously implanted in BALB/c nude mice, and to determine the expression levels of Bax and Bcl-2 in tumor tissues and to explore the mechanism of action. Methods: A subcutaneous xenograft model was established in nude mouse K562 cells. The mice were sacrificed by continuous intraperitoneal administration for 12 days. Nude mice were sacrificed. The tumor mass was weighed and the tumor inhibition rate was calculated. HE staining and transmission electron microscopy were used to observe the apoptosis of tumor cells. Immunohistochemistry was used to observe the expression of Bax and Bcl-2 protein in tumor tissues. RT-PCR was used to detect the mRNA levels of Bax and Bcl-2 in tumor tissues. . Results: The anti-tumor effect of each drug group was significantly different from that of the negative control group (P<0.05). The high-dose group had the same anti-tumor effect as the hydroxyurea group (P>0.05). It was found by light and electron microscopy. Apoptosis and necrosis of tumor cells were observed in the emodin low, middle and high concentration groups, and the highest concentration was observed in the high concentration treatment group. Some tumor cells in the hydroxyurea treatment group were mainly necrotic. The results of immunohistochemistry and RT-PCR showed that the expression of Bax and Bax mRNA was up-regulated and the expression of Bcl-2 and Bcl-2 mRNA was down-regulated in emodin-treated tumors. CONCLUSION: Emodin can significantly inhibit the growth of K562 cells in nude mice. Its mechanism may be through regulating the expression of Bax and Bcl-2 in tumors, thereby promoting apoptosis.