1. 南京中医药大学第一临床医学院
2. 江苏省中医药防治肿瘤协同创新中心
纸质出版:2018
移动端阅览
[1]饶希午,沈卫星,谭佳妮,徐长亮,孙东东,杨烨,史丽云,程海波.消癌解毒方对肝癌模型大鼠血清蛋白差异表达的蛋白质组学研究[J].中医杂志,2018,59(22):1953-1958.
RAO Xiwu, SHEN Weixing, TAN Jiani, et al. Proteomic Analysis Study on Effects of Xiaoai Jiedu Decoction(消癌解毒方) on Expressions of Serum Differential Proteins in Liver Cancer Model Rats[J]. Journal of Traditional Chinese Medicine2018, 59(22): 1953-1958.
[1]饶希午,沈卫星,谭佳妮,徐长亮,孙东东,杨烨,史丽云,程海波.消癌解毒方对肝癌模型大鼠血清蛋白差异表达的蛋白质组学研究[J].中医杂志,2018,59(22):1953-1958. DOI: 10.13288/j.11-2166/r.2018.22.013.
RAO Xiwu, SHEN Weixing, TAN Jiani, et al. Proteomic Analysis Study on Effects of Xiaoai Jiedu Decoction(消癌解毒方) on Expressions of Serum Differential Proteins in Liver Cancer Model Rats[J]. Journal of Traditional Chinese Medicine2018, 59(22): 1953-1958. DOI: 10.13288/j.11-2166/r.2018.22.013.
目的探讨消癌解毒方治疗肝癌的可能作用机制。方法 40只雄性SD大鼠随机分为正常组、模型组和消癌解毒方低剂量组、高剂量组各10只。模型组与消癌解毒方低剂量组、高剂量组大鼠自由饮用0. 01%二乙基亚硝胺(DEN)溶液建立肝癌模型。消癌解毒方低剂量组、高剂量组大鼠于造模第4周给予剂量为10. 87、21. 74 g/(kg·d)的消癌解毒方溶液灌胃
模型组给予生理盐水2 ml/d灌胃
每周6天
共12周。第16周取肝脏组织进行形态学观察
检测肝脏重量并计算脏器系数;取血清样本进行蛋白质串联质谱标签(TMT)肽段标记
质谱鉴定
应用KOBAS 3. 0软件分析差异表达蛋白质的生物信息学。结果共鉴定到1151个蛋白点。模型组与正常组差异表达明显的蛋白共234个
其中上调蛋白151个
下调蛋白83个。消癌解毒方低剂量组与模型组差异表达明显的蛋白共144个
包括上调蛋白56个
下调蛋白88个。消癌解毒方高剂量组与模型组差异表达明显的蛋白共182个
包括上调蛋白94个
下调蛋白88个。消癌解毒方高剂量组差异表达蛋白主要参与了代谢、炎症反应、免疫调控、热休克、氧化应激、细胞周期与凋亡、细胞生长与分化、血管生成、癌相关、肝再生修复等。信号通路分析涉及谷胱甘肽代谢、过氧化物酶体增殖剂激活受体(PPAR)代谢等代谢相关通路
细胞外基质受体相互作用通路、Toll样受体(TLRs)通路、低氧诱导因子1 (HIF-1)通路、核因子κB (NF-κB)通路、哺乳动物雷帕霉素靶蛋白(m TOR)通路、p53通路等。结论消癌解毒方可对肝癌大鼠发挥多系统、多靶点参与的整体调控作用
其中调控炎癌转变可能是其抑制肿瘤发生发展的主要作用机制。
Objective To observe the effects and probable mechanism of Xiaoai Jiedu Decoction(消癌解毒方) in treating liver cancer rat. Methods A total of 40 male Sprague-Dawley rats were randomly divided into normal group
model group
Xiaoai Jiedu Decoction low and high dose groups
with 10 rats in each group. The rats in the low and high Xiaoai Jiedu Decoction dose groups and model group were treated with 0. 01% diethylnitrosamine(DEN) solution for free drinking to establish liver cancer models. The Xiaoai Jiedu Decoction low dose group and high dose group respectively received 10. 87 g/(kg·d) and 21. 74 g/(kg·d) Xiaoai Jiedu Decoction solution for gavage administration at the 4 th week while the model group received 2 ml/d normal saline
6 days a week for 12 weeks. Liver tissues of all rats were taken for morphological observation at the end of the 16 th week. The liver weight was measured
and the organ coefficient was calculated. The samples were labeled with protein tandem mass tag(TMT) peptide segment
identified by the mass spectrometry
and the bioinformatics was analyzed by KOBAS 3. 0 software.Results A total of 1151 protein spots were identified. Compared with the normal group
there were 234 proteins which differentially expressed in the model group
including 151 up-regulated proteins and 83 down-regulated proteins. Compared with the model group
there were 144 differentially expressed proteins in the Xiaoai Jiedu Decoction low-dose group
including 56 up-regulated proteins and 88 down-regulated proteins. Compared with the model group
there were 182 differentially expressed proteins in the Xiaoai Jiedu Decoction high-dose group
including 94 up-regulated proteins and 88 down-regulated proteins. These differentially expressed proteins in Xiaoai Jiedu Decoction highdose group mainly involved in metabolism
inflammation
immune regulation
heat shock
oxidative stress
cell cycle and apoptosis
cell growth and differentiation
angiogenesis
cancer-related and liver regeneration repair. Signaling pathway analysis involved metabolic pathways
such as glutathione metabolism
peroxisome proliferator-activated receptors(PPAR) metabolism
extracellular matrix receptor interaction(ECM-receptor-interaction) pathway
Toll-like receptors(TLRs) pathway
hypoxia-inducible factors-1(HIF-1) pathway
nuclear factor-κB(NF-κB)
mammalian target of rapamycin(m TOR) pathway
and p53 pathway. Conclusion Xiaoai Jiedu Decoction can play a multisystem
multi-target participation in the overall regulation of liver cancer model rats
regulation to inflammation-cancer transmisson may be the main mechanism of its inhibition of tumorigenesis and development.
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