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目的研究放射治疗诱发BALB/c小鼠Renca肾癌细胞凋亡的特点及其调控机制,为肿瘤放射治疗提供实验依据。方法采用Annexin-V-FITC/PI法流式细胞仪检测不同剂量放疗后细胞凋亡率,建立BALB/c小鼠肾癌细胞肿瘤种植模型,采用PV免疫组织化学法检测肿瘤石蜡切片P53的表达及ELISA试剂盒检测细胞因子IL-2、IFN-γ的表达。结果①在一定照射剂量范围内,Renca细胞的凋亡率随剂量的增加而升高。②放疗组突变型P53蛋白表达率为(30.17±0.88)%,肿瘤组为(24.22±0.68)%,两组间有显著的统计学差异。③放疗组小鼠脾细胞分泌IL-2为(167.56±13.13)pg/mL,为肿瘤组小鼠分泌量(83.69±1.37)pg/mL的2倍,两组间有显著的统计学差异。放疗组小鼠脾细胞分泌IFN-γ为(1482.47±47.91)pg/mL,约为肿瘤组小鼠分泌量(211.02±35.98)pg/mL的7倍,两组间有显著的统计学差异。结论放疗可诱发Renca细胞凋亡,P53蛋白可能涉及本实验中的细胞凋亡通路。
Objective To study the characteristics and regulatory mechanism of radiation-induced apoptosis in Renca’s renal cell carcinoma of the BALB / c mice and provide experimental evidence for radiotherapy of tumor. Methods Annexin-V-FITC / PI flow cytometry was used to detect the rate of apoptosis after radiotherapy with different doses of radiotherapy. BALB / c mouse kidney cancer cell model was established. The expression of P53 in tumor paraffin sections was detected by PV immunohistochemistry ELISA kit was used to detect the expression of cytokines IL-2 and IFN-γ. Results ① The apoptosis rate of Renca cells increased with the increase of dose at certain irradiation dose. ② The expression of mutant P53 protein in radiotherapy group was (30.17 ± 0.88)%, (24.22 ± 0.68)% in tumor group, with significant difference between the two groups. ③ The secretion of IL-2 in the spleen cells in radiotherapy group was (167.56 ± 13.13) pg / mL, which was twice as much as that in the tumor group (83.69 ± 1.37 pg / mL). There was significant difference between the two groups. The IFN-γ secreted by spleen cells of mice in radiotherapy group was (1482.47 ± 47.91) pg / mL, which was about 7 times higher than that in tumor group (211.02 ± 35.98) pg / mL. There was significant difference between the two groups. Conclusion Radiation therapy can induce Renca cell apoptosis. P53 protein may be involved in the apoptotic pathway in this experiment.