基于Caspase-1/IRAKs/NF-κB信号通路的健脾治法对肝癌大鼠抑制作用及机制分析  

Analysis on Inhibitory Effect and Mechanism of Spleen-Strengthening Therapy on Liver Cancer Rats Based on Caspase-1/IRAKs/NF-κB Signaling Pathway

作　　者：蒋筱 罗淑娟 卓少元 JIANG Xiao;LUO Shujuan;ZHUO Shaoyuan(School of Basic Medicine,Guangxi University of Chinese Medicine,Nanning 530000,Guagnxi,China;Faculty of Chinese Medicine Science,Guangxi University of Chinese Medicine,Nanning 530000,Guagnxi,China)

机构地区：[1]广西中医药大学基础医学院,广西南宁530000 [2]广西中医药大学赛恩斯新医药学院,广西南宁530000

出　　处：《中华中医药学刊》2023年第1期182-185,共4页Chinese Archives of Traditional Chinese Medicine

基　　金：广西自然科学基金面上项目(2018GXNSFAA281045);广西高校中青年教师基础能力提升项目(2019KY1078);广西中医药大学广西一流学科建设项目重点课题(2018XK015)。

摘　　要：目的分析基于Caspase-1/白细胞介素1受体相关激酶(interleukin 1 receptor-associated kinases,IRAKs)/核因子κB(nuclear factorκB,NF-κB)信号通路的健脾治法对肝癌大鼠抑制作用及机制。方法选取90只雄性SD大鼠,使用随机数字表法分为对照组、模型组、研究组,各30只,模型组、研究组均以二乙基亚硝胺(diethylnitrosamine,DEN)诱导原发性肝癌模型,对照组予等量生理盐水处理。建模16周后给予研究组健脾治法处理。对比3组大鼠建模16周后、建模18周后、建模20周后肝功能、肝脏病理学及肝细胞Caspase-1、IRAKs、NF-κB信号通路相关蛋白变化,分析健脾治法的肝癌抑制作用及机制。结果对照组建模16周~建模20周脏器指数,血清甲胎蛋白(alpha-fetoprotein,AFP)、谷草转氨酶(aspartate transaminase,AST)、谷丙转氨酶(alanine aminotrans,ALT)、Caspase-1、IRAK-1、IRAK-4、NF-κB mRNA表达均未见明显变化(P>0.05);模型组、研究组建模16周后脏器指数,AFP、AST、ALT,Caspase-1、IRAK-1、IRAK-4、NF-κB mRNA表达均高于对照组(P<0.05);模型组建模18周、建模20周后脏器指数,AFP、AST、ALT,Caspase-1、IRAK-1、IRAK-4、NF-κB mRNA表达均高于建模16周(P<0.05);研究组建模18周、建模20周脏器指数,AFP、AST、ALT,Caspase-1、IRAK-1、IRAK-4、NF-κB mRNA表达均低于建模16周(P<0.05)。与建模16周相比,模型组建模18周、建模20周肝脏组织病变程度升高,研究组建模18周、建模20周肝脏组织病变程度降低(P<0.05)。结论肝癌发生发展伴随着Caspase-1、IRAKs、NF-κB信号通路增强,基于健脾治法对肝癌大鼠进行干预,能够抑制Caspase-1、IRAKs、NF-κB信号通路,从而改善肝癌大鼠肝功能、缓解肝脏病理学改变。Objective To analyze the inhibitory effect and mechanism of spleen-strengthening therapy based on Caspase-1/interleukin-1 receptor-associated kinases(IRAKs)/nuclear factorκB(NF-κB)signaling pathway on liver cancer rats.Methods A total of 90 male SD rats were selected and divided into control group,model group and study group with 30 rats in each group by random number table method.The primary liver cancer model of model group and study group were induced with diethylnitrosamine(DEN),and the control group was treated with the same amount of normal saline.16 weeks after modeling,the study group was treated with spleen-strengthening treatment.The changes of liver function,liver pathology and proteins related to Caspase-1,IRAKs and NF-κB signaling pathway in liver cells after 16,18 and 20 weeks of modeling were compared among the three groups,and the inhibitory effect and mechanism of spleen-strengthening therapy on liver cancer were analyzed.Results There were no significant changes in expressions of alpha-fetoprotein(AFP),aspartate transaminase(AST),alanine aminotrans(ALT),Caspase-1,IRAK-1,IRAK-4 or NF-κB mRNA in the control group from 16 to 20 weeks after modeling(P>0.05).The expressions of AFP,AST,ALT,Caspase-1,IRAK-1,IRAK-4 and NF-κB mRNA in model group and study group were higher than those in control group 16 weeks after modeling(P<0.05).The mRNA expressions of AFP,AST,ALT,Caspase-1,IRAK-1,IRAK-4 and NF-κB were all higher at 18 weeks and 20 weeks after modeling than those at 16 weeks(P<0.05).The expressions of AFP,AST,ALT,Caspase-1,IRAK-1,IRAK-4 and NF-κB mRNA in the study group at 18 and 20 weeks after modeling was lower than that at 16 weeks(P<0.05).Compared with 16 weeks of modeling,the degree of liver lesion increased at 18 and 20 weeks of modeling,and the degree of liver lesion decreased in the study group at 18 and 20 weeks of modeling(P<0.05).Conclusion The occurrence and development of liver cancer is accompanied by the enhancement of Caspase-1,IRAKs and NF-κB signaling pathways.Intervention ba

关 键 词：CASPASE-1 白细胞介素1受体相关激酶 核转录因子ΚB 肝癌 

分 类 号：R285.5[医药卫生—中药学]