目的 觀察杠板歸對小鼠H22肝癌的抑制作用，分析其可能的作用機制。方法 建立H22皮下移植小鼠模型評價杠板歸對腫瘤生長的影響；二甲苯誘導的耳腫脹評價杠板歸對荷瘤小鼠炎癥的影響；網(wǎng)絡藥理學分析杠板歸抗腫瘤和抗炎可能的作用機制。結(jié)果 杠板歸對H22皮下腫瘤生長有明顯抑制作用（P<0.05），顯著降低二甲苯誘導的荷瘤小鼠耳腫脹（P<0.05）。通過上海有機所化學專業(yè)數(shù)據(jù)庫以口服生物利用度（OB）≥30%和類藥性（DL）≥0.18篩選杠板歸4種有效成分，與生物芯片肝癌上下調(diào)基因蛋白分子對接得到106個預測靶點，預測靶點與TTD比對得到13個肝癌治療靶點。蛋白相互作用網(wǎng)絡（PPI）分析STAT3、IL-6、IL-1β、HBG2、TLR4、HBB、HBE1、HBD為8個核心靶點，其參與27個KEGG通路和27個生物過程。結(jié)論 杠板歸對小鼠H22肝癌有抑制作用，能減輕荷瘤小鼠炎癥，其作用與4個活性成分參與“泛素化介導蛋白水解”、“核因子（NF）-κB信號傳導”、“Janus激酶-信號轉(zhuǎn)導與轉(zhuǎn)錄激活子（JAK-STAT）信號傳導”等通路有關(guān)。

Objective To observe the inhibitory effect of Polygonum perfoliatum L. on H22 liver carcinoma in mice and explore its possible action mechanisms. Methods Effect of Polygonum perfoliatum L. on tumor growth was evaluated using H22 subcutaneously transplanted tumor model in mice, effect of Polygonum perfoliatum L on inflammation was examined by ear edema in tumor bearing mice. Network pharmacology was used to analyze the possible action mechanisms by which Polygonum perfoliatum L. exerts anti-tumor and anti-inflammation efficacy. Results Polygonum perfoliatum L. had an anti-tumor effect on H22 liver carcinoma in mice and obviously decreased xylene-induced ear edema in tumor-bearing mice(P<0.05). 4 active components with OB ≥ 30%and DL ≥ 0.18 in Shanghai Institute of Organic Chemistry database, and up-and-down genes of liver cancer in the biochip were selected for molecular docking. 106 predicted targets were compared to liver cancer therapeutic targets in TTD, there were 13 liver cancer therapeutic targets related with four active components. PPI analysis indicates that STAT3, IL6, IL1B, HBG2, TLR4, HBB, HBE1, HBD are 8 core targets which involve in 27 KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways and 27 GO (gene ontology) biological process. Conclusion Polygonum perfoliatum L. has an inhibitory effect on H22 liver cancer and could decrease inflammation in tumor bearing mice, its action mechanisms are associated 4 active components which involve in "ubiquitination-mediated proteolysis", "NF-κB signaling", and "JAK-STAT signaling", et al pathway.

河南省自然科學基金項目（182300410310）