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目的:观察蝎毒多肽(PESV)干预NOD/SCID小鼠模型体内慢性粒细胞白血病(CML)bcr-abl融合基因及p210、p53、TNF-α、bcl-xl表达水平变化。方法:应用K562细胞注入经过铯-137源照射270cGy的NOD/SCID小鼠体内,建立CML NOD/SCID小鼠模型;对实验小鼠随机分组,用Real-time PCR检测PESV治疗后小鼠体内bcrabl融合基因表达水平,ELISA法检测小鼠p210、p53、TNF-α、bcl-xl表达水平。结果:PESV能够抑制模型小鼠体内bcr-abl融合基因及p210表达水平,能够提升p53表达,抑制TNF-α、bcl-xl过度表达,其抑制效果与PESV浓度具有相关性。结论:PESV通过干预CML bcr-abl融合基因和其表达的p210,影响细胞凋亡信号传导通路途径,有效地阻断CML传变进展,揭示了PESV干预CML传变的微观机制。
Objective: To observe the changes of bcr-abl fusion gene and the expression of p210, p53, TNF-α and bcl-xl in the NOD / SCID mouse model induced by scorpion venom polypeptide (PESV). Methods: The mouse model of CML NOD / SCID was established by injecting K562 cells with NO2 / SCID mice exposed to cesium-137 source at a dose of 270 cGy. The mice were randomly divided into groups. Real-time PCR was used to detect the bcrabl Fusion gene expression levels, ELISA p210, p53, TNF-α, bcl-xl expression levels. Results: PESV could inhibit the expression of bcr-abl fusion gene and p210 in model mice, increase the expression of p53 and inhibit the overexpression of TNF-α and bcl-xl. The inhibitory effect was related to the concentration of PESV. CONCLUSIONS: PESV can effectively block the progression of CML transformation by intervening the fusion gene of bcr-abl and its expression of p210 in PESV, and reveal the microscopic mechanism of PESV intervention in CML transformation.