基于PI3K/Akt信号途径探讨理气消瘿方对结节性甲状腺肿大鼠的作用机制

Study on the mechanism of Liqi Xiaoying Recipe on rats with nodular goiter based on PI3K/Akt signal pathway

目的基于PI3k/Akt信号途径探析理气消瘿方对结节性甲状腺肿大鼠的机制研究。方法60只Wist-ar雄性大白鼠,随机分为空白对照组、模型组、优甲乐组、消瘿方组,每组15只。空白对照组坚持每日进行普通胃喂养并给予生理盐水灌胃,模型组完成造模后同样给予生理盐水灌胃,优甲乐组给予优甲乐溶液灌服,消瘿方组给予活血消瘿方灌服。比较四组大鼠PI3K、Akt信号通路分子表达量以及1个月内存活情况。结果空白对照组PI3K信号通路分子表达量为(1.00±0.01)低于模型组的(1.52±0.07)、优甲乐组的(1.41±0.07)、消瘿方组的(1.31±0.08),差异均具有统计学意义(t=28.482、22.457、14.892,P<0.05)。消瘿方组PI3K信号通路分子表达量明显低于模型组及优甲乐组,差异均有统计学意义(t=7.651、3.643,P<0.05)。空白对照组Akt信号通路分子表达量为(1.00±0.01)低于模型组的(2.14±0.08)、优甲乐组的(2.01±0.03)、消瘿方组的(1.67±0.07),差异均具有统计学意义(t=54.764、123.70、36.697,P<0.05)。消瘿方组Akt信号通路分子表达量均低于模型组、优甲乐组,差异均具有统计学意义(t=17.124、12.388,P<0.05)。空白对照组小鼠存活率100.00%明显高于模型组的33.33%、优甲乐组的53.33%,差异均具有统计学意义(P<0.05);空白对照组与消瘿方组大鼠存活率比较,差异无统计学意义(P<0.05)。结论结节性甲状腺肿的发生可能与PI3K/Akt信号通路蛋白分子表达量上调有关联,临床给予消瘿方治疗可抑制PI3KAkt信号通路激活达到一定治疗目的。

Objective To study the mechanism of Liqi Xiaoying Recipe on rats with nodular goiter based on PI3 K/Akt signal pathway. Methods A total of 60 Wistar male rats were randomly divided into blank control group, model group, Youjiale group and Xiaoying Recipe group, with 15 rats in each group. The blank control group was given normal gastric feeding and normal saline gavage every day, the model group was given normal saline gavage after modeling, the Youjiale group was given Youjiale solution gavage, the Xiaoying Recipe group was given Huoxue Xiaoying Recipe gavage. The expressions of PI3K and Akt signaling pathway molecules and the survival of rats in 1 month were compared among the four groups. Results The expressions of PI3 K signaling pathway molecules of blank control group was(1.00±0.01), which was lower than(1.52±0.07) of model group,(1.41±0.07) of Youjiale group and(1.31±0.08) of Xiaoying Recipe group, and the difference was statistically significant(t=28.482, 22.457, 14.892;P<0.05). The expressions of PI3 K signaling pathway molecules of Xiaoying Recipe group was obviously lower than those of model group and Youjiale group, and hte difference was statistically significant(t=7.651, 3.643;P<0.05). The expressions of Akt signaling pathway molecules of blank control group was(1.00±0.01), which was lower than(2.14±0.08) of model group,(2.01±0.03) of Youjiale group and(1.67±0.07) of Xiaoying Recipe group, and the difference was statistically significant(t=54.764, 123.70, 36.697;P<0.05). The expressions of Akt signaling pathway molecules of Xiaoying Recipe group was lower than those of model group and Youjiale group, and the difference was statistically significant(t=17.124, 12.388;P<0.05). The rat survival rate 100.00% of blank control group was obviously higher than 33.33% of model group and 53.33% of Youjiale group, and the difference was statistically significant(P<0.05). There was no statistically significant difference in rat survival rate between blank control group and Xiaoying Recipe group(P<0.05). Conclusion The occurrence of nodular goiter may be related to the up-regulation of protein expression in PI3K/Akt signaling pathway. Clinical administration of Xiaoying Recipe can inhibit the activation of PI3K/Akt signaling pathway to achieve certain therapeutic goals.