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目的观察芪莲舒痞方对慢性萎缩性胃炎癌前病变大鼠突变型p53、脾酪氨酸激酶(Syk)、Survivin表达的影响,探讨芪莲舒痞方的作用机理。方法采用“MNNG+雷尼替丁+乙醇+饥饱失调”的综合方法复制Wistar大鼠CAG癌前病变模型,按随机数字表法分为正常组、模型组、芪莲舒痞(QLSP)大、中、小剂量组和胃复春(WFC)组,分别给予药物干预后,免疫组化S-P法检测突变型p53、Syk、Survivin的表达。结果 (1)突变型p53表达:除QLSP大剂量组外,其余各组突变型p53蛋白阳性表达率较正常组均显著增强(P<0.01);QLSP大剂量组、WFC组突变型p53蛋白阳性表达率较模型组显著降低(P<0.01或P<0.05)。(2)Syk表达:模型组、WFC组、QLSP中、小剂量组Syk阳性表达率较正常组显著减少(P<0.01);QLSP大剂量组Syk阳性表达率较模型组显著增多(P<0.01)。(3)Survivin表达:胃复春组、QLSP大剂量组Survivin阳性表达率较模型组显著减弱(P<0.05或P<0.01)。结论芪莲舒痞方能抑制突变型p53、Survivin的表达,增强Syk的表达,这可能是其逆转CAG癌前病变的作用机制之一。
Objective To observe the effect of Qi Lian Shu Zu Fang on the expression of mutant p53, Syk and Survivin in rats with chronic atrophic gastritis precancerous lesions and to explore the mechanism of Qilian Shu Rui Fang. Methods Wistar rat model of CAG precancerous lesion was duplicated by the comprehensive method of “MNNG + ranitidine + ethanol + hunger and blood loss”, and divided into normal group, model group, QLSP, Large, medium and low dose groups and WFC group were given drug intervention, immunohistochemical SP method to detect mutant p53, Syk, Survivin expression. Results (1) Mutant p53 expression: In addition to QLSP high-dose group, the positive rate of mutant p53 protein in other groups were significantly increased (P <0.01); QLSP high-dose group, WFC group of mutant p53 protein positive The expression rate was significantly lower than the model group (P <0.01 or P <0.05). (2) Syk expression: The Syk positive expression rate in model group, WFC group and QLSP middle-small dose group was significantly lower than that in normal group (P <0.01); Syk positive rate in QLSP high dose group was significantly higher than that in model group (P <0.01) ). (3) The expression of Survivin: Compared with the model group, the positive expression rate of Survivin in the Wefuchun group and QLSP high dose group was significantly weaker (P <0.05 or P <0.01). Conclusion Qilianshupuri can inhibit the expression of mutant p53 and Survivin, and enhance the expression of Syk, which may be one of the mechanisms of reversing CAG precancerous lesions.