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Abstract：
UNASSIGNED: This study aims to elucidate anti-liver cancer components and potential mechanisms of Curcumae Rhizoma and Hedyotis diffusa Willd (CR-HDW).
UNASSIGNED: Effective components and targets of CR-HDW were identified from the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database. Liver cancer-related genes were collected from GeneCards, Gene-Disease Association (DisGeNET), and National Center for Biotechnology Information (NCBI). Protein-protein interaction networks, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment were conducted to analyze the identified genes. Molecular docking was used to simulate binding of the active components and their target proteins. Cell activity assay, western blot, and senescence-associated β-galactosidase (SA-β-gal) experiments were conducted to validate core targets identified from molecular docking.
UNASSIGNED: Ten active compounds of CR-HDW were identified including quercetin, 3-epioleanic acid and hederagenin. The primary core proteins comprised Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), Protein Kinase B(AKT1), etc. The pathways for Phosphoinositide 3-kinase (PI3K)/ AKT, cellular senescence, Fork head boxO (FOXO) were revealed as important for anti-cancer activity of CR-HDW. Molecular docking demonstrated strong binding between liver cancer target proteins and major active components of CR-HDW. In-vitro experiments confirmed that hederagenin and 3-epioleolic acid inhibited HuH-7 cell growth, reduced expression of PI3K, AKT, and mechanistic target of rapamycin (mTOR) proteins. Hederagenin also induced HuH-7 senescence.
UNASSIGNED: In summary, The authors\' results suggest that the CR-HDW component (Hederagenin, 3-epoxy-olanolic acid) can inhibit the proliferation of HuH-7 cells by decreasing PI3K, AKT, and mTOR. Hederagenin also induced HuH-7 senescence.
UNASSIGNED: Effective components and targets of CR-HDW were identified from the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database. Liver cancer-related genes were collected from GeneCards, Gene-Disease Association (DisGeNET), and National Center for Biotechnology Information (NCBI). Protein-protein interaction networks, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment were conducted to analyze the identified genes. Molecular docking was used to simulate binding of the active components and their target proteins. Cell activity assay, western blot, and senescence-associated β-galactosidase (SA-β-gal) experiments were conducted to validate core targets identified from molecular docking.
UNASSIGNED: Ten active compounds of CR-HDW were identified including quercetin, 3-epioleanic acid and hederagenin. The primary core proteins comprised Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), Protein Kinase B(AKT1), etc. The pathways for Phosphoinositide 3-kinase (PI3K)/ AKT, cellular senescence, Fork head boxO (FOXO) were revealed as important for anti-cancer activity of CR-HDW. Molecular docking demonstrated strong binding between liver cancer target proteins and major active components of CR-HDW. In-vitro experiments confirmed that hederagenin and 3-epioleolic acid inhibited HuH-7 cell growth, reduced expression of PI3K, AKT, and mechanistic target of rapamycin (mTOR) proteins. Hederagenin also induced HuH-7 senescence.
UNASSIGNED: In summary, The authors\' results suggest that the CR-HDW component (Hederagenin, 3-epoxy-olanolic acid) can inhibit the proliferation of HuH-7 cells by decreasing PI3K, AKT, and mTOR. Hederagenin also induced HuH-7 senescence.
摘要：
■本研究旨在阐明姜黄和白花蛇舌草（CR-HDW）的抗肝癌成分和潜在机制。
■从中药系统药理学(TCMSP)数据库鉴定了CR-HDW的有效组分和靶标。从GeneCards收集肝癌相关基因，基因疾病协会（DisGeNet），国家生物技术信息中心（NCBI）。蛋白质-蛋白质相互作用网络，进行基因本体论(GO)和京都基因和基因组百科全书(KEGG)富集以分析鉴定的基因。分子对接用于模拟活性组分与其靶蛋白的结合。细胞活性测定,westernblot,进行了衰老相关的β-半乳糖苷酶（SA-β-gal）实验，以验证从分子对接中确定的核心靶标。
■鉴定出10种CR-HDW活性化合物，包括槲皮素，3-表油酸和海得草素。主要核心蛋白包括甘油醛-3-磷酸脱氢酶（GAPDH），蛋白激酶B(AKT1),等。磷酸肌醇3-激酶（PI3K）/AKT的途径，细胞衰老,叉头盒O(FOXO)被揭示为对于CR-HDW的抗癌活性重要。分子对接显示肝癌靶蛋白与CR-HDW的主要活性成分之间的强结合。体外实验证实，hederagenin和3-表油酸抑制HuH-7细胞生长，降低PI3K的表达，AKT,和雷帕霉素（mTOR）蛋白的机制靶标。Hederagenin也诱导HuH-7衰老。
■总之，作者的结果表明，CR-HDW成分(Hederagenin，3-环氧-齐墩果酸）可以通过降低PI3K来抑制HuH-7细胞的增殖，AKT,还有MTOR.Hederagenin也诱导HuH-7衰老。
■从中药系统药理学(TCMSP)数据库鉴定了CR-HDW的有效组分和靶标。从GeneCards收集肝癌相关基因，基因疾病协会（DisGeNet），国家生物技术信息中心（NCBI）。蛋白质-蛋白质相互作用网络，进行基因本体论(GO)和京都基因和基因组百科全书(KEGG)富集以分析鉴定的基因。分子对接用于模拟活性组分与其靶蛋白的结合。细胞活性测定,westernblot,进行了衰老相关的β-半乳糖苷酶（SA-β-gal）实验，以验证从分子对接中确定的核心靶标。
■鉴定出10种CR-HDW活性化合物，包括槲皮素，3-表油酸和海得草素。主要核心蛋白包括甘油醛-3-磷酸脱氢酶（GAPDH），蛋白激酶B(AKT1),等。磷酸肌醇3-激酶（PI3K）/AKT的途径，细胞衰老,叉头盒O(FOXO)被揭示为对于CR-HDW的抗癌活性重要。分子对接显示肝癌靶蛋白与CR-HDW的主要活性成分之间的强结合。体外实验证实，hederagenin和3-表油酸抑制HuH-7细胞生长，降低PI3K的表达，AKT,和雷帕霉素（mTOR）蛋白的机制靶标。Hederagenin也诱导HuH-7衰老。
■总之，作者的结果表明，CR-HDW成分(Hederagenin，3-环氧-齐墩果酸）可以通过降低PI3K来抑制HuH-7细胞的增殖，AKT,还有MTOR.Hederagenin也诱导HuH-7衰老。
