《中国中药杂志》：“中医药对癌症功效机制”主题双语文案保举-外链论坛

j8typz 发表于 2024-6-23 23:57:03

《中国中药杂志》：“中医药对癌症功效机制”主题双语文案保举

<img src="//q1.itc.cn/images01/20240527/2817169c9f334e2b8f4385ffaf3655a8.jpeg" style="width: 50%; margin-bottom: 20px;">
围绕中医药对癌症的功效机制科研，本期精选发布在《中国中药杂志》的5篇双语文案，期盼能为关联行业学者供给新的思路与参考，欢迎阅读。
精选文案Selected Articles
01
柴胡-白芍含药血液经过miR-1297/PTEN信号轴对HepG2肝癌细胞的影响及机制科研
Bupleuri Radix-Paeoniae Radix Alba medicated plasma exerts effects on HepG2 hepatoma cells by regulating miR-1297/PTEN signaling axis
【摘要】科研柴胡-白芍含药血液经过微小RNA-1297（microRNA-1297，miR-1297）/第10号染色体缺失的磷酸酶及张力蛋白同源基因（phosphatase and tensin homologue deleted on chromosome 10，PTEN）信号轴对肝癌细胞HepG2的影响及功效机制。经过实时荧光定量聚合酶链反应（real-time quantitative PCR，RT-qPCR）检测miR-1297、PTEN mRNA在肝癌细胞株中的表达，双荧光素酶报告实验验证miR-1297与PTEN的靶向关系。将HepG2肝癌细胞分为空白血液组、含药血液组、miR-1297 inhibitor组、miR-NC组、miR-1297 inhibitor+含药血液组。细胞计数试剂（CCK-8）法检测细胞增殖，筛选含药血液最佳干涉浓度即时间。细胞划痕实验和Transwell实验检测细胞迁移、侵袭能力，碘化丙啶（PI）染色法检测细胞周期分布，Annexin V-FITC/PI双染法检测细胞凋亡水平。RT-qPCR检测miR-1297、PTEN、蛋白激酶B（Akt）、磷脂酰肌醇3-激酶（PI3K）基因表达。蛋白免疫印迹（Western blot，WB）检测PTEN、PI3K、磷酸化磷脂酰肌醇3-激酶（p-PI3K）、Akt、磷酸化蛋白激酶B（p-Akt）、半胱氨酸蛋白酶3（caspase-3）、半胱氨酸蛋白酶9（caspase-9）、B淋巴细胞瘤-2（Bcl-2）、Bcl-2关联X蛋白（Bax）的蛋白表达。结果表示，miR-1297在HepG2细胞中表达水平最高，选择HepG2细胞进行后续实验。双荧光素酶报告实验表示miR-1297可与PTEN mRNA3′-非翻译区（3′-untranslated region，3′UTR）结合。柴胡-白芍含药血液能够控制HepG2细胞增殖，最佳干涉质量分数即时间为20%、72 h。与空白血液组相比，含药血液组、miR-1297 inhibitor组及miR-1297 inhibitor+含药血液组均能控制HepG2细胞增殖、侵袭及迁移，能够加强G0/G1期细胞比例，降低S期细胞比例，加强细胞凋亡率。柴胡-白芍含药血液能够降低HepG2细胞miRNA-1297、PI3K、Akt mRNA表达，加强PTEN mRNA表达；能够下调p-PI3K、p-Akt、Bcl-2蛋白表达；上调PTEN、caspase-3、caspase-9、Bax的蛋白表达。综上，柴胡、白芍能够控制HepG2肝癌细胞miR-1297的表达，上调PTEN表达，负调控PI3K/Akt信号通路，从而控制HepG2细胞增殖并诱导凋亡。
【Abstract】The present study is designed to investigate the effect and mechanism of Bupleuri Radix-Paeoniae Radix Alba medicated plasma on HepG2 hepatoma cells by regulating the microRNA-1297 (miR-1297)/phosphatase and tensin homologue deleted on chromosome 10 (PTEN) signaling axis. Real-time quantitative PCR (RT-qPCR) was carried out to determine the mRNA levels of miR-1297 and PTEN in different hepatoma cell lines. The dual luciferase reporter assay was employed to verify the targeted interaction between miR-1297 and PTEN. The cell counting kit-8 (CCK-8) was used to detect cell proliferation. Optimal concentration and intervention time of the medicated plasma were determined. The cell invasion and migration were examined by Transwell experiment and wound healing assay. Cell cycle distribution was detected by PI staining. Apoptosis of cells was detected by Annexin V-FITC/PI double staining. The mRNA levels of miR-1297, PTEN, protein kinase B (Akt), and phosphatidylinositol 3-kinase (PI3K) were determined by RT-qPCR. Western blot was employed to determine the protein levels of PTEN, Akt, p-Akt, caspase-3, caspase-9, B-cell lymphoma-2 (Bcl-2), and Bcl-2-associated X protein (Bax). The results showed that HepG2 cells were the best cell line for subsequent experiments. In the dual luciferase reporter assay, it is confirmed that miR-1297 can combine with the 3′-untranslated region (3′UTR) in the mRNA of PTEN. The medicated plasma has inhibited the proliferation of HepG2 cells. Optimal intervention concentration and time are 20% and 72 h. Compared with the blank plasma, the Bupleuri Radix-Paeoniae Radix Alba medicated plasma, miR-1297 inhibitor, miR-1297 inhibitor + medicated plasma all can inhibit the proliferation, invasion, and migration of HepG2 cells, and increase the proportion of cells in the G0/G1 phase. The proportion of cells in the S phase has been decreased. The apoptosis rate can be increased. The medicated plasma can down-regulate the mRNA levels of miR-1297, PI3K, and Akt. It also can upregulate the mRNA level of PTEN. In addition, it has up-regulated the protein levels of PTEN, Bax, caspase-3, and caspase-9, and down-regulated the protein levels of p-Akt, p-PI3K, and Bcl-2. In conclusion, Bupleuri Radix-Paeoniae Radix Alba medicated plasma can inhibit the expression of miR-1297 in HepG2 hepatoma cells, and promote the expression of PTEN. Thus, it can negatively regulate PI3K/Akt signaling pathway, to inhibit the proliferation and induce the apoptosis of HepG2 cells.
02
黄芪-莪术药对经过调控缺氧诱导因子及肿瘤干细胞化控制结肠癌发展并加强5-FU疗效的机制科研
Astragali Radix-Curcumae Rhizoma inhibits colon cancer progression and enhances 5-FU efficacy by regulating hypoxia-inducible factors and tumor stem cells
【摘要】该科研基于动物和细胞模型科研黄芪-莪术药对经过调控缺氧诱导因子及肿瘤干细胞化控制结肠癌发展并加强5-氟尿嘧啶（5-FU）疗效的机制。创立裸鼠HCT116皮下移植瘤模型，将造模成功的24只裸鼠随机分为模型组、5-FU组、黄芪-莪术组和联合给药组，治疗后每2 d测绘1次肿瘤体积，采用Western blot办法检测裸鼠HCT116皮下移植瘤组织缺氧核心区重要靶点表皮生长因子受体（epidermal growth factor receptor，EGFR）、二氢嘧啶脱氢酶(dihydropyrimidine dehydrogenase, DPYD)、胸苷酸合酶（thymidylate synthase，TYMS）以及缺氧诱导因子-1α（hypoxia-inducible factor-1α，HIF-1α）、缺氧诱导因子-2α（hypoxia-inducible factor-2α，HIF-2α）和肿瘤干细胞标志物CD133、SRY盒转录因子2（SRY-box transcription factor 2，SOX2）的蛋白表达状况。结果显示黄芪-莪术药对能减缓肿瘤生长速度，并明显加强5-FU的抑瘤率。黄芪-莪术药对显著降低肿瘤中EGFR和DPYD的蛋白表达，联合给药组中EGFR和TYMS的蛋白表达量明显降低。与模型组相比，黄芪-莪术药对能够明显控制移植瘤组织缺氧核心区中HIF-1α、HIF-2α、SOX2、CD133的蛋白表达，与5-FU组相比，联合给药进一步控制了HIF-1α、HIF-2α、SOX2的蛋白表达。在体外实验中，缺氧后HCT116细胞内HIF-1α、HIF-2α的蛋白表达量明显增多。与单独给予5-FU（1.38μmol·L-1）相比，单独运用黄芪-莪术（40 mg·mL-1）或5-FU联合黄芪-莪术均能更明显地控制HIF-1α、HIF-2α、TYMS的蛋白表达。结果表示黄芪-莪术药对降低了结肠癌细胞中缺氧应答分子的表达，并减少了结肠癌的干细胞性质，从而起到了协同加强5-FU对结肠癌的治疗功效。
【Abstract】The animal and cell models were used in this study to investigate the mechanism of Astragali Radix-Curcumae Rhizoma (HQEZ) in inhibiting colon cancer progression and enhancing the efficacy of 5-fluorouracil (5-FU) by regulating hypoxia-inducible factors and tumor stem cells. The animal model was established by subcutaneous transplantation of colon cancer HCT116 cells in nude mice, and 24 successfully modeled mice were randomized into the model, 5-FU, HQEZ, and 5-FU+HQEZ groups. The tumor volume was measured every two days. Western blot was employed to measure the protein levels of epidermal growth factor receptor (EGFR), dihydropyrimidine dehydrogenase (DPYD), and thymidylate synthase (TYMS), the key targets of the hypoxic core region, as well as the hypoxia-inducible factors HIF-1 α and HIF-2 α and the cancer stem cell surface marker CD133 and SRY-box transcription factor 2 (SOX2). The results of animal experiments showed that HQEZ slowed down tumor growth and significantly increased the tumor inhibition rate of 5-FU. Compared with the model group, HQEZ significantly down-regulated the protein levels of EGFR and DPYD, and 5-FU+HQEZ significantly down-regulated the protein levels of EGFR and TYMS in tumors. Compared with the model group, HQEZ significantly down-regulated the protein levels of HIF-1 α, HIF-2 α, SOX2, and CD133 in the hypoxic core region. Compared with the 5-FU group, 5-FU+HQEZ lowered the protein levels of HIF-1 α, HIF-2 α, and SOX2. The cell experiments showed that the protein levels of HIF-1 α and HIF-2 α in HCT116 cells elevated significantly after low oxygen treatment. Compared with 5-FU (1.38 1.38 μmol·L -1) alone, HQEZ (40 mg·mL -1) and 5-FU+HQEZ significantly down-regulated the protein levels of HIF-1 α, HIF-2 α, and TYMS. In conclusion, HQEZ can inhibit the expression of hypoxia-responsive molecules in colon cancer cells and reduce the properties of cancer stem cells, thereby enhancing the therapeutic effect of 5-FU on colon cancer.
03
榅桲总多酚经过PI3K/Akt/mTOR通路影响肾癌细胞增殖和迁移
Total polyphenols of Cydonia oblonga inhibited proliferation and migration of renal cancer cells by PI3K/Akt/mTOR pathway
【摘要】经过网络药理学与生物信息学及实验验证相结合的办法来阐明榅桲总多酚（total polyphenols of Cydonia oblonga Miller，TPCOM）抗肾癌的功效机制。经过网络药理学筛选榅桲活性多酚类化合物和肾癌关联的靶点。经过对Gene Expression Omnibus（GEO）数据库中肾癌病人肿瘤组织和正常组织RNA测序数据进行差异表达基因分析，结合网络药理学预测结果和差异表达基因分析得到TPCOM功效于肾癌的核心基因，结合存活分析找出能够影响病人存活的重要靶点，进行京都基因与基因组百科全书（Kyoto Encyclopedia of Genes and Genomes，KEGG）和基因本体（Gene Ontology，GO）富集分析。采用20～640μg·mL-1 TPCOM处理786-O和Renca细胞进行cell counting kit-8（CCK-8）实验，40、80、160μg·mL-1 TPCOM处理肾癌细胞，检测TPCOM对肾癌细胞迁移和肾癌细胞中蛋白激酶B（protein kinase B，Akt）、雷帕霉素靶蛋白（mammalian target of rapamycin，mTOR）和磷脂酰肌醇3-激酶（phosphoinositide 3-kinase，PI3K）信号通路关联蛋白表达水平的调控功效。经过网络药理学预测得到8个榅桲多酚类活性化合物，经过存活分析得到TPCOM发挥抗肾癌功效的15个明显影响病人存活的肾癌差异表达基因。KEGG和GO分析结果表示以上15个靶点重点与PI3K/Akt信号通路、细胞迁移和增殖等生物过程相关。结果表示TPCOM能够控制786-O和Renca细胞的增殖，IC50分别为121.4、137.9μg·mL-1。TPCOM能够控制786-O和Renca细胞的迁移，能够控制PI3K/Akt/mTOR信号通路。榅桲总多酚可能经过控制PI3K/Akt/mTOR信号通路的激活从而控制肾癌细胞的增殖和迁移来发挥抗肾癌功效。该科研为新疆天然产物榅桲的抗肿瘤功效科研供给必定的科研基本，对进一步推动新疆榅桲的研发和利用拥有拓展和弥补道理。
【Abstract】The mechanism of total polyphenols of Cydonia oblonga Miller (TPCOM) against kidney cancer was elucidated through a combination of network pharmacology, bioinformatics, and experimental verification. The active polyphenolic compounds from C. oblonga were screened by network pharmacological techniques and kidney cancer-related targets were collected through the database. The differential gene expression analysis was performed on RNA sequencing data from tumor tissue and normal tissue of kidney cancer patients obtained from the Gene Expression Omnibus (GEO) database. The results of network pharmacology predictions and differential gene expression analysis were used to identify the core genes targeted by TPCOM in kidney cancer. Survival analysis was conducted to identify key targets that could impact patient survival, followed by Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analyses. Cell proliferation and activity experiments (cell counting kit-8) were conducted using TPCOM at concentrations ranging from 20 to 640 μg·mL −1 on 786-O and Renca cells. Additionally, TPCOM at concentrations of 40, 80, and 160 μg·mL −1 was applied to kidney cancer cells to assess its effect on cell migration and its regulation of protein expression levels related to the protein kinase B (Akt), mammalian target of rapamycin (mTOR), and phosphoinositide 3-kinase (PI3K) signaling pathways. Network pharmacology predicted eight active polyphenolic compounds from C. oblonga. Survival analysis revealed 15 significantly differentially expressed genes in kidney cancer that were affected by TPCOM and had a significant impact on patient survival. KEGG and GO analysis results indicated that these 15 targets were primarily associated with the PI3K/Akt signaling pathway, cell migration, and proliferation. The results showed that TPCOM could inhibit the proliferation of 786-O and Renca cells, with IC 50 values of 121.4 and 137.9 μg·mL −1, respectively. TPCOM was also found to inhibit the migration of these cells and suppress the PI3K/Akt/mTOR signaling pathway. TPCOM may exert its anti-kidney cancer effects by inhibiting the activation of the PI3K/Akt/mTOR signaling pathway, thereby restraining the proliferation and migration of kidney cancer cells. This study provides a foundation for the research on the anti-tumor effects of natural product C. oblonga, particularly in Xinjiang, and holds significance for further promoting its development and utilization.
 04
芹菜素与氧化苦参碱联合用药控制非小细胞肺癌的功效及其机制科研
Effect of apigenin in combination with oxymatrine on non-small cell lung cancer and mechanism
【摘要】科研芹菜素、氧化苦参碱、芹菜素与氧化苦参碱联合给药（以下简叫作“联合给药”）对非小细胞肺癌细胞系的增殖功效及其分子功效机制的影响。采用CCK-8法检测芹菜素、氧化苦参碱以及联合给药对非小细胞肺癌A549与NCI-H1975细胞活力的影响；经过平板克隆实验考察芹菜素、氧化苦参碱以及联合给药后对非小细胞肺癌细胞克隆形成能力的影响；EdU实验验证芹菜素、氧化苦参碱以及联合给药对非小细胞肺癌NCI-H1975细胞增殖率的影响；RT-qPCR与Western blot实验考察芹菜素、氧化苦参碱以及联合给药后对PLOD2 mRNA与蛋白相对表达的影响；分子对接实验探究芹菜素、氧化苦参碱与PLOD2、EGFR蛋白的直接功效能力与功效位点；利用Western blot法检测芹菜素、氧化苦参碱以及联合给药对EGFR下游信号通路关联蛋白表达水平的影响。结果发掘，芹菜素、联合给药在20、40、80μmol·L-1均能明显控制人非小细胞肺癌A549与NCI-H1975细胞的活力并呈浓度依赖性；芹菜素、联合给药功效于NCI-H1975细胞可明显控制非小细胞肺癌细胞的克隆形成能力；芹菜素以及联合给药后可明显控制PLOD2的mRNA与蛋白相对表达；芹菜素、氧化苦参碱与PLOD2、EGFR蛋白有较强的结合功效；芹菜素、联合给药可明显下调非小细胞肺癌细胞EGFR及其下游信号通路蛋白表达水平。联合给药能控制非小细胞肺癌，且其功效机制可能与EGFR及其下游信号通路关联。该科研为芹菜素与氧化苦参碱联合应用治疗非小细胞肺癌供给科学依据，对联合给药抗肿瘤功效机制的深入科研拥有必定的参考道理。
【Abstract】This study explored the effect of apigenin (APG), oxymatrine (OMT), and APG + OMT on the proliferation of the non-small cell lung cancer cell lines and the underlying mechanism. Cell counting kit-8 (CCK-8) assay was used to detect the vitality of A549 and NCI-H1975 cells, and colony formation assay to evaluate the colony formation ability of the cells. EdU assay was employed to examine the proliferation of NCI-H1975 cells. RT-qPCR and Western blot were performed to detect the mRNA and protein expression of PLOD2. Molecular docking was carried out to explore the direct action ability and action sites between APG/OMT and PLOD2/EGFR. Western blot was used to study the expression of related proteins in the EGFR pathway. The viability of A549 and NCI-H1975 cells was inhibited by APG and APG + OMT at 20, 40, and 80 μmol·L −1 in a dose-dependent manner. The colony formation ability of NCI-H1975 cells was significantly suppressed by APG and APG + OMT. The mRNA and protein expression of PLOD2 was significantly inhibited by APG and APG + OMT. In addition, APG and OMT had a strong binding activity with PLOD2 and EGFR. In APG and APG + OMT groups, the expression of EGFR and proteins in its downstream signaling pathways was significantly down-regulated. It is concluded that APG in combination with OMT could inhibit non-small lung cancer, and the mechanism may be related to EGFR and its downstream signaling pathways. This study lays a new theoretical basis for the clinical treatment of non-small cell lung cancer with APG in combination with OMT and provides a reference for further research on the anti-tumor mechanism of APG in combination with OMT.
05
基于网络药理学及体外实验验证探讨乌药抗胃癌的功效机制
Mechanism of Linderae Radix against gastric cancer based on network pharmacology and in vitro experimental validation
【摘要】利用网络药理学、分子对接技术和体外细胞实验，科研乌药抗胃癌的重点活性成份和潜在功效机制。利用中药系统药理学分析平台（TCMSP）数据库、在线人类孟德尔遗传（OMIM）和GeneCards数据库提取乌药活性成份，并预测了乌药与胃癌相关靶点。筛选二者一起的潜在功能靶位之后，再利用STRING数据库实现与二者一起靶点的蛋白相互功效（PPI）网络构建。利用DAVID数据库进行GO和KEGG富集分析；以STRING和DAVID数据库为基本，运用Cytoscape 3.7.2软件构建“活性成份-靶点”网络和“活性成份-靶点-通路”网络；利用AutoDock Vina进行分子对接，预测有效成分与重要功效靶点的结合度，最后对重要靶点和通路进行体外实验验证。预测结果共得到乌药活性成份9个、关联靶点179个，乌药与胃癌的一起靶点107个，靶点共触及生物过程693种，细胞构成57种，分子功能129种，参与肿瘤抗原p53、缺氧诱导因子1等信号通路161条；分子对接结果表示核心成份吉马酮与TP53有较高的结合活性。最后体外实验将筛选出的乌药活性成份吉马酮对人胃癌细胞SGC-7901进行核心靶点和通路的初步验证，结果显示吉马酮可显著控制胃癌细胞增殖并经过调控p53、Bax、Bcl-2等重要蛋白的表达来诱导SGC-7901凋亡。综上所述，乌药经过多成份、多靶点、多通路协同功效掌控胃癌的出现发展，为今后临床进一步探讨乌药治疗胃癌的机制供给理论依据。
【Abstract】The present study explored the main active ingredients and the underlying mechanism of Linderae Radix in the treatment of gastric cancer by network pharmacology, molecular docking, and in vitro cell experiments. TCMSP, OMIM and GeneCards databases were used to obtain the active ingredients of Linderae Radix to predict the related targets of both Linderae Radix and gastric cancer. After screening of the common potential action targets, the STRING database was used to construct the PPI network for protein interaction of the common targets. Enrichment analysis of GO and KEGG was performed by DAVID database. Based on STRING and DAVID platform data, Cytoscape software was used to construct an “active ingredient–target” network and an “active ingredient–target–pathway” network. Molecular docking was performed using AutoDock Vina to predict the binding of the active components to the key action targets, and finally the key targets and pathways were verified in vitro. According to the prediction results, there were 9 active components, 179 related targets of Linderae Radix, 107 common targets of Linderae Radix and gastric cancer, 693 biological processes, 57 cellular components, and 129 molecular functions involved in the targets, and 161 signaling pathways involved in tumor antigen p53, hypoxia-inducible factor 1, etc. Molecular docking found that the core component, germacrone had high binding activity with TP53. Finally, in an in vitro experiment, the screened active ingredient of Linderae Radix germacrone was used for preliminarily verifying the core targets and pathways of the human gastric cancer cell SGC-7901. The results showed that germacrone could significantly inhibit the proliferation of gastric cancer cells and induce the apoptosis of SGC-7901 by regulating the expression of p53, Bax, Bcl-2 and other key proteins. In summary, Linderae Radix can control the occurrence and development of gastric cancer through multi-components, multi-targets and multi-pathways, which will provide theoretical basis for further clinical discussion on the mechanism of Linderae Radix in treating gastric cancer.
期刊举荐Recommended Journal
<img src="//q4.itc.cn/images01/20240527/f9e5fa4c5dcb42c0a38707e222e966bd.jpeg" style="width: 50%; margin-bottom: 20px;">
《中国中药杂志》是由于中国科学技术协会主管，中国药学会主办，中国中医科学院中药科研所承办的综合性中医药学术期刊，创刊于1955年7月，现为半月刊，全年24期，每期240页。全面反映我国中医药与天然药品学科行业最新发展与科研动态，是中医药最高研究学术水平的交流平台之一。名誉主编肖培根院士、王永炎院士、张伯礼院士、屠呦呦科研员。现任主编为中国工程院黄璐琦院士。入选中国中医药科技期刊分级目录T1区，名列11本T1级期刊榜首；中文核心期刊；中国科技核心期刊；中国科学引文数据库（CSCD核心版）Q1区；中国学术期刊（网络版）源自期刊。在国际上，被Medline《生物医学检索系统》（美）、Scopus《文摘与引文数据库》（荷兰）、BP《生物学文摘(预评)》（美）、IPA《国际药学文摘》（美）、JST日本科学技术振兴公司数据库（日）等数据库收录。
联系咱们Contact Us 
<img src="//q7.itc.cn/images01/20240527/f9cb6a054216456c805fc129b3dfdb8b.png" style="width: 50%; margin-bottom: 20px;">
中国知网“中文精品学术期刊外文版数字出版工程”（简叫作JTP）自2015年起步，已与400余种学术期刊合作出版了5万余篇双语对照论文，累积了丰富的学术翻译/英语加工/学术推广经验。形成为了集双语出版、主题电子书出版、双语讲座视频制作、期刊英文内容编校加工、资讯编译、海外推广为一体的全方位服务体系，全面助力期刊提高国际影响力。感兴趣的伴侣请联系<a style="color: black;">返回外链论坛：http://www.fok120.com/，查看更加多</a>

责任编辑：网友投稿

b1gc8v 发表于 2024-9-30 01:24:53

你的留言真是温暖如春，让我感受到了无尽的支持与鼓励。

4zhvml8 发表于 2024-9-30 18:23:13

感谢你的精彩评论，带给我新的思考角度。

页: [1]

外链论坛's Archiver

《中国中药杂志》：“中医药对癌症功效机制”主题双语文案保举