灰树花多糖联合顺铂对肺癌模型小鼠p38 MAPK/ATF2信号通路调控作用的实验研究

Experimental Study on Regulation of p38 MAPK/ATF2 Signaling Pathway in Lung Cancer Model Mice Were Treated by Grifola Frondosa Polysaccharide Combined with Cisplatin

目的 观察顺铂联合灰树花多糖对Lewis肺癌小鼠的抑瘤作用,并阐述其抑制p38/ATF2信号通路过表达的作用机制.方法 45 只小鼠随机分为3组,模型对照组(n=15),顺铂组(n=15),顺铂联合灰树花组(n=15).3组小鼠均经左腋下皮下注射Lewis细胞悬液0.2 mL,即每只小鼠接种细胞数为105 个.1 周后观察成瘤情况并开始对顺铂组和顺铂联合灰树花组进行相应药物干预,连续2 周.末次给药后,处死小鼠,测量肿瘤组织重量,以及瘤组织中p38、p-p38、ATF-2的表达水平.结果 与模型对照组比较,顺铂组及顺铂联合灰树花组小鼠肿瘤重量显著减轻,肿瘤组织中p38、p-p38、ATF-2的表达水平显著降低,差异有统计学意义(P<0.01);与顺铂组比较,顺铂联合灰树花组小鼠瘤重显著减轻,瘤组织中p38、p-p38、ATF-2的表达水平显著降低,差异有统计学意义(P<0.01).结论 顺铂与灰树花多糖联合应用,对Lewis种植瘤小鼠模型具有明显的抑瘤作用,其作用机制可能是通过抑制p38/ATF2信号的过度活化而实现的.

Objective To observe the tumor-suppressive effect of cisplatin combined with Grifola frondosa polysaccharide on mice with Lewis lung cancer, and to elucidate the mechanism of inhibition of overexpression of p38/ATF2 signaling pathway. Methods 45 mice were randomly divided into three groups: model control group (n=15), cisplatin group (n=15) and cisplatin combined with Grifola frondosa polysaccharides group (n=15). All the mice in the three groups were injected with 0.2 mL Lewis cell suspension subcutaneously under the left armpit, that is, 105 cells were inoculated in each mouse. After one week, the tumorigenesis was observed and the corresponding drug intervention was started in the cisplatin group and cisplatin combined with Grifola frondosa polysaccharides group for 2 consecutive weeks. After the final administration, mice were sacrificed to measure the weight of tumor tissues and the expression levels of p38, p-p38 and ATF-2 in tumor tissues. Results Compared with the model control group, the tumor weight of the mice in the cisplatin guoup and cisplatin combined with Grifola frondosa polysaccharides group was significantly reduced, and the expression levels of p38, p-p38 and ATF-2 in tumor tissues were significantly reduced, showing a statistical difference (P<0.01). Compared with cisplatin group, the tumor weight of mice in the cisplatin combined with Grifola frondosa polysaccharides group was significantly reduced, and the expression levels of p38, p-p38, and ATF-2 in the tumor tissues were significantly reduced, with statistically significant differences (P<0.01). Conclusion Joint application of Grifola frondosa polysaccharide on Lewis growing tumor mouse model has obvious tumor suppression effect, its mechanism may be achieved by inhibiting the excessive activation of p38/ATF2 signaling pathway.