PDF(Pubmed)
Abstract：
UNASSIGNED: Traditional Chinese medicine (TCM) therapy is an important means to treat hepatocellular carcinoma (HCC), Astragalus (Latin name: Hedysarum Multijugum Maxim; Chinese name: Huangqi, HQ) and Atractylodes (Latin name: Atractylodes Macrocephala Koidz; Chinese name: Baizhu, BZ) (HQBZ), a classic herb pair, is often used in combination to HCC. However, the main components and potential mechanisms of HQBZ therapy in HCC remain unclear. This study aimed to identify the potential active ingredients and molecular mechanisms of action of HQBZ in HCC treatment.
UNASSIGNED: The HQBZ-Compound-Target-HCC network and HQBZ-HCC transcriptional regulatory network were constructed to screen the core active compound components and targets of HQBZ therapy for HCC. Molecular docking techniques are used to verify the stability of binding core active compound components to targets. GO and KEGG enrichment analysis were used to explore the signaling pathway of HQBZ in HCC treatment, the mechanism of HQBZ treatment of HCC was verified based on in vivo H22 tumor bearing mice and in vitro cell experiments.
UNASSIGNED: Network pharmacology and molecular docking studies showed that HQBZ treatment of HCC was related to the targeted regulation of IL-6 and STAT3 by the active compound biatractylolide, KEGG pathway enrichment analysis suggest that HQBZ may play a role in the treatment of HCC through IL-6/STAT3 signaling pathway. In vitro experiment results proved that HQBZ could regulate IL-6/STAT3 signaling pathway transduction on CD8+T cells, inhibit CD8+T cell exhaustion and restore the function of exhausted CD8+T cells. In vivo experiment results proved that HQBZ can regulate IL-6/STAT3 signaling pathway transduction in H22 liver cancer model mouse tumor tissue, increased the proportion of tumor infiltrating CD8+T cells.
UNASSIGNED: This study found that HQBZ may play a therapeutic role in HCC by targeting IL-6 and STAT3 through biatractylolide, its mechanism of action is related to regulating IL-6/STAT3 signaling pathway, reversing T cell failure and increasing tumor infiltration CD8+T cells.
UNASSIGNED: The HQBZ-Compound-Target-HCC network and HQBZ-HCC transcriptional regulatory network were constructed to screen the core active compound components and targets of HQBZ therapy for HCC. Molecular docking techniques are used to verify the stability of binding core active compound components to targets. GO and KEGG enrichment analysis were used to explore the signaling pathway of HQBZ in HCC treatment, the mechanism of HQBZ treatment of HCC was verified based on in vivo H22 tumor bearing mice and in vitro cell experiments.
UNASSIGNED: Network pharmacology and molecular docking studies showed that HQBZ treatment of HCC was related to the targeted regulation of IL-6 and STAT3 by the active compound biatractylolide, KEGG pathway enrichment analysis suggest that HQBZ may play a role in the treatment of HCC through IL-6/STAT3 signaling pathway. In vitro experiment results proved that HQBZ could regulate IL-6/STAT3 signaling pathway transduction on CD8+T cells, inhibit CD8+T cell exhaustion and restore the function of exhausted CD8+T cells. In vivo experiment results proved that HQBZ can regulate IL-6/STAT3 signaling pathway transduction in H22 liver cancer model mouse tumor tissue, increased the proportion of tumor infiltrating CD8+T cells.
UNASSIGNED: This study found that HQBZ may play a therapeutic role in HCC by targeting IL-6 and STAT3 through biatractylolide, its mechanism of action is related to regulating IL-6/STAT3 signaling pathway, reversing T cell failure and increasing tumor infiltration CD8+T cells.
摘要：
■中医治疗是治疗肝细胞癌的重要手段,黄芪（拉丁名：HedysarumMultijumgumMaxim；中文名：黄芪，HQ)和白术(拉丁名:白术;中文名:白术,BZ)(HQBZ)，一对经典的草药,通常与HCC结合使用。然而,HQBZ治疗HCC的主要成分和潜在机制尚不清楚。本研究旨在确定HQBZ在HCC治疗中的潜在活性成分和作用分子机制。
■构建了HQBZ-Compound-Target-HCC网络和HQBZ-HCC转录调控网络，以筛选HQBZ治疗HCC的核心活性化合物成分和靶标。分子对接技术用于验证结合核心活性化合物组分与靶标的稳定性。采用GO和KEGG富集分析探讨HQBZ在HCC治疗中的信号通路,通过体内H22荷瘤小鼠和体外细胞实验验证了HQBZ治疗HCC的机制。
■网络药理学和分子对接研究表明，HQBZ治疗HCC与活性化合物Biatractylide对IL-6和STAT3的靶向调节有关，KEGG通路富集分析提示HQBZ可能通过IL-6/STAT3信号通路在HCC治疗中发挥作用。体外实验结果证明HQBZ能够调节IL-6/STAT3信号通路对CD8+T细胞的转导,抑制CD8+T细胞耗尽，恢复耗尽的CD8+T细胞的功能。体内实验结果证明,HQBZ可以调节H22肝癌模型小鼠肿瘤组织中IL-6/STAT3信号通路的转导,增加肿瘤浸润CD8+T细胞的比例。
■这项研究发现，HQBZ可能通过比曲内酯靶向IL-6和STAT3在HCC中发挥治疗作用，其作用机制与调节IL-6/STAT3信号通路,逆转T细胞衰竭和增加肿瘤浸润CD8+T细胞。
■构建了HQBZ-Compound-Target-HCC网络和HQBZ-HCC转录调控网络，以筛选HQBZ治疗HCC的核心活性化合物成分和靶标。分子对接技术用于验证结合核心活性化合物组分与靶标的稳定性。采用GO和KEGG富集分析探讨HQBZ在HCC治疗中的信号通路,通过体内H22荷瘤小鼠和体外细胞实验验证了HQBZ治疗HCC的机制。
■网络药理学和分子对接研究表明，HQBZ治疗HCC与活性化合物Biatractylide对IL-6和STAT3的靶向调节有关，KEGG通路富集分析提示HQBZ可能通过IL-6/STAT3信号通路在HCC治疗中发挥作用。体外实验结果证明HQBZ能够调节IL-6/STAT3信号通路对CD8+T细胞的转导,抑制CD8+T细胞耗尽，恢复耗尽的CD8+T细胞的功能。体内实验结果证明,HQBZ可以调节H22肝癌模型小鼠肿瘤组织中IL-6/STAT3信号通路的转导,增加肿瘤浸润CD8+T细胞的比例。
■这项研究发现，HQBZ可能通过比曲内酯靶向IL-6和STAT3在HCC中发挥治疗作用，其作用机制与调节IL-6/STAT3信号通路,逆转T细胞衰竭和增加肿瘤浸润CD8+T细胞。
