摘要
目的研究八月札乙醇提取物体内对H22肝癌细胞增殖、促进凋亡及对PI3K/Akt信号通路的影响。方法构建小鼠H22肝癌皮下移植瘤模型,随机分为模型组、5-氟脲嘧啶(5-Fu)组、八月札乙醇提取物高、中、低剂量组,每组12只,模型组灌胃给予等体积的生理盐水,八月札乙醇提取物高、中、低剂量组分别灌胃给予40、20、10生药g/kg,5-Fu组腹腔注射5-Fu 0.02 g/kg,1次/d,连续给药10 d。每天观察并记录荷瘤小鼠基本情况;末次给药后分离瘤块,测量瘤体体积、称瘤体质量及计算抑瘤率;分别采用免疫组织化学法和Western blot法检测八月札乙醇提取物对瘤组织中PI3K、Akt、Bcl-xL和Bad及Caspase-9蛋白表达的影响。结果八月札乙醇提取物各给药组小鼠的基本情况均优于模型组;与模型组比,5-Fu组和八月札乙醇提取物高、中、低剂量组瘤体体积和体质量均明显减少(P<0.05或P<0.01);八月札乙醇提取物高、中、低剂量组对H22小鼠肝癌皮下移植瘤模型具有明显的抑瘤作用,抑瘤率分别为62.3%、58.5%和55.7%;并能显著下调肿瘤组织中PI3K和Bcl-xL蛋白表达,显著上调Bad和Caspase-9的蛋白表达(P<0.01),Akt在各组瘤组织中表达差异无统计学意义(P>0.05)。结论八月札乙醇提取物具有体内抑制H22细胞增殖、促进H22细胞凋亡的作用,其机制可能与抑制PI3K/Akt信号通路活化有关。
Objective o investigate the effect of ethanol extract of Bayuezha[Akebia trifoliata(Thunb.)Koidz.](EEATK)on the proliferation and apoptosis of H22 liver cancer cell of mice via PI3 K/Akt signaling pathway in vivo.Methods The subcutaneous xenograft model of H22 liver cancer cells in mice was established,the mice were randomly divided into model group,5-fluorouracil(5-Fu)treatment group and EEATK high,medium and low dose groups,with 12 mice in each group.The model group was given the equal volume normal saline by intragastric administration.The 5-Fu treatment group was intraperitoneally injected 5-Fu(0.02 g/kg).EEATK high,medium and low dose groups were administered with EEATK 40,20,10 crude drug g/kg respectively.Each group was given the corresponding drug once a day for 10 days.During the administration,the mice were monitored and recorded daily to obverse the situation of the mice.After the last administration,the tumor tissues were dissected,measured and weighted to calculate the tumor inhibition rate.The expressions of phosphoinositide 3-kinase(PI3 K),protein kinase B(AKT),Bcl-xl,Bad and Caspase-9 protein in tumor tissues by were detected by immunohistochemical staining and western blot respectively.Results The situations of mice in EEATK high,medium and low dose groups were better than those in the model group.Compared with those of model group,the volumes and weights of tumors were decreased in the 5-Fu treatment group and EEATK high,medium and low dose groups(P<0.05 or P<0.01).The experimental results showed that EEATK had significant tumor-inhibiting effect.The inhibitory rate of EEATK high,medium and low dose groups were 62.3%,58.5%and 55.7%,respectively.EEATK could not only significantly decrease the expressions of PI3 K and Bcl-xl in the tumor tissue but also significantly increase the expressions of Bad and Caspase-9 proteins(P<0.01).Conclusion EEATK can inhibit H22 cells proliferation and promote H22 apoptosis in vivo.The mechanism may be related to inhibiting the activation of PI3 K/Akt signaling pat
作者
王春玲
张瑜
文晓东
郑作文
WANG Chunling;ZHANG Yu;WEN Xiaodong;ZHENG Zuowen(Department of Pharmacy,Guangxi University of Chinese Medicine,Nanning 530200,Guangxi,China;Jiangsu Easy-Immun Biotechnology Co.Ltd,Wuxi 214142,Jiangsu,China;Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine,Nanning 530011,Guangxi,China)
出处
《中华中医药学刊》
CAS
北大核心
2022年第9期73-77,I0021,I0022,共7页
Chinese Archives of Traditional Chinese Medicine
基金
国家自然科学基金(82060888)
广西高校中药药理重点实验室项目(J14045)。
