固本抑瘤Ⅱ号抑制Hep-2荷瘤小鼠喉癌发生的机制研究  

A Study on the Mechanism of Guben YiliuⅡInhibiting Pathogenesy of Laryngeal Cancer in Hep-2 Tumor Bearing Mice

作　　者：白云飞[1] 崔晓波[1] 王博谦 王亚平[1] 杨莉娜 刘佳荣 覃洁[1] BAI Yun-fei;CUI Xiao-bo;WANG Bo-qian;WANG Ya-ping;YANG Li-na;LIU Jia-rong;QIN Jie(Department of Otolaryngology,the Affiliated Hospital of Inner Mongolia Medical University,Hohhot 010050,China)

机构地区：[1]内蒙古医科大学附属医院耳鼻咽喉科,呼和浩特010050

出　　处：《解放军医药杂志》2021年第9期11-16,共6页Medical & Pharmaceutical Journal of Chinese People’s Liberation Army

基　　金：内蒙古自然科学基金(2017MS0839)。

摘　　要：目的探究固本抑瘤Ⅱ号(GYⅡ)抑制Hep-2荷瘤小鼠喉癌发生的作用机制。方法构建Hep-2异种移植裸鼠模型,并采用随机数字表法分为模型组、GYⅡ2.5 g/kg组和GYⅡ5.0 g/kg组,每组5只。GYⅡ不同剂量组灌胃法给药,模型组灌胃等量生理盐水,每日1次,连续30 d。处理过程中,每3天测量肿瘤体积1次,结束后剥离小鼠瘤体并拍照;采用流式细胞术测定细胞凋亡率;TUNEL凋亡染色检测瘤体凋亡细胞数量;Western blot法检测瘤体组织中ERK和Akt蛋白磷酸化水平。结果至实验终点,GYⅡ2.5 g/kg组和GYⅡ5.0 g/kg组肿瘤体积均小于模型组,GYⅡ5.0 g/kg组肿瘤体积小于GYⅡ2.5 g/kg组,差异有统计学意义(P<0.01)。GYⅡ2.5 g/kg组和GYⅡ5.0 g/kg组肿瘤细胞凋亡率及凋亡细胞数量均高于模型组,GYⅡ5.0 g/kg组亦高于GYⅡ2.5 g/kg组,差异有统计学意义(P<0.01)。GYⅡ2.5 g/kg组和GYⅡ5.0 g/kg组肿瘤组织中p-ERK和p-Akt蛋白表达量较模型组低,且GYⅡ5.0 g/kg组低于GYⅡ2.5 g/kg组,差异有统计学意义(P<0.01)。结论GYⅡ可显著抑制ERK和Akt信号通路活性,促进肿瘤细胞凋亡,从而达到抑制肿瘤生长的作用,有望成为喉癌患者有效的辅助治疗方剂。Objective To explore the mechanism of Guben YiliuⅡ(GYⅡ)in inhibition of pathogenesy of laryngeal cancer in Hep-2 tumor bearing mice.Methods Xenograft models of Hep-2 in nude mice were established and divided into model group(n=5),GYⅡ2.5 g/kg group(n=5)and GYⅡ5.0 g/kg group(n=5)according to random number table method.GYⅡ2.5 g/kg and 5.0 g/kg groups were given GYⅡby intragastric administration,while model group was given the same volume of normal saline by once a day for consecutive 30 d.During the treatment,tumor volumes were measured by every 3 days.After the treatment,tumors were stripped and photographed,and apoptosis rates were detected by flow cytometry.TUNEL apoptosis staining was used to detect numbers of apoptotic cells,and expressions of ERK and Akt phosphorylated proteins were detected by Western blot.Results At the end of the experiment,tumor volumes in GYⅡ2.5 g/kg and GYⅡ5.0 g/kg groups were significantly smaller than that in model group,and the tumor volume in GYⅡ5.0 g/kg group was significantly smaller than that in GYⅡ2.5 g/kg group(P<0.01).Values of apoptosis rates and numbers of apoptotic cells in GYⅡ2.5 g/kg and GYⅡ5.0 g/kg groups were significantly higher than those in model group,and the values in GYⅡ5.0 g/kg group were significantly higher than those in GYⅡ2.5 g/kg group(P<0.01).Protein expressions of p-ERK and p-Akt in tumor tissues in GYⅡ2.5 g/kg and GYⅡ5.0 g/kg groups were significantly lower than those in model group,and the expressions in GYⅡ5.0 g/kg group were significantly lower than those in GYⅡ2.5 g/kg group(P<0.01).Conclusion GYⅡmay inhibit tumor growth by significantly inhibiting the activities of ERK and Akt signaling pathways and promoting the apoptosis of tumor cells,and therefore,it is expected to become an effective adjuvant therapy for patients with laryngeal cancer.

关 键 词：喉肿瘤 小鼠 固本抑瘤Ⅱ号 中草药 ERK AKT 

分 类 号：R739.65[医药卫生—肿瘤] R-332[医药卫生—临床医学]