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丹尼尔抑制肺腺癌的机制。

Mechanism of Daniell. Inhibiting Lung Adenocarcinoma.

作者信息

Chen Qi, Liu Tingting, Bai Tuya, Zhang Mengdi, Hu Yuxia, Li Jun, Chang Fuhou

机构信息

School of Pharmacy, Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region, China.

New Drug Safety Evaluation Research Center, Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region, China.

出版信息

Evid Based Complement Alternat Med. 2022 Feb 12;2022:5242179. doi: 10.1155/2022/5242179. eCollection 2022.

DOI:10.1155/2022/5242179
PMID:35190747
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8858071/
Abstract

: Daniell. (SD) is a natural plant fruit and is famous for containing miraculin. It has been reported that SD can be used as an adjuvant treatment to correct patients' loss of taste during the antitumor process, but the effect of SD itself as an antitumor is not clear. In this study, we investigated the mechanism of action of SD on lung adenocarcinoma using network pharmacology. . The components of SD were identified by liquid chromatography-mass spectrometry, and then the compounds that affect tumor immunity of SD were screened and the related targets were predicted by TCMIO database. At the same time, the results were associated with lung adenocarcinoma targets included in the MalaCards and CTD databases, so as to construct a compound-target action network diagram and explore the mechanism of SD in the treatment of lung adenocarcinoma. In in vitro experiments, cell viability was determined and western blotting was used to detect the related expression of action targets to determine the therapeutic effect of SD. . In this experiment, 335 chemical components were identified in SD, and 107 components were related to tumor immunity. After screening by ADME, it was found that 11 compounds might be inhaled into the human body and affect the growth of lung adenocarcinoma. In vitro experiments showed that SD could inhibit the growth of lung adenocarcinoma A549 cells. SD could reduce the expression of PCNA ( < 0.05) and significantly increase the expression of Caspase-3 ( < 0.05). The results of further experiments showed that SD could significantly reduce the phosphorylation of EGFR ( < 0.05), and SD could also effectively inhibit the expression of JAK and STAT3 phosphorylation ( < 0.01) and inhibit the expression of PI3K and AKT phosphorylation ( < 0.01). . SD can inhibit the growth of lung adenocarcinoma A549 cells and the potential mechanism was found to be the inhibition of EGFR/JAK/STAT3 and EGFR/PI3K/AKT signaling pathway, and the substance basis for SD to exert antitumor effect may be catechin, taxifolin, betaine, epigallocatechin gallate, erucamide, guanosine, kaempferol, lanosterol, morin, oleanolic acid, and quercetin.

摘要

丹尼尔(SD)是一种天然植物果实,以含有 miraculin 而闻名。据报道,SD 可作为辅助治疗来纠正患者在抗肿瘤过程中味觉丧失的情况,但 SD 本身作为抗肿瘤药物的效果尚不清楚。在本研究中,我们使用网络药理学研究了 SD 对肺腺癌的作用机制。通过液相色谱 - 质谱法鉴定了 SD 的成分,然后筛选出影响 SD 肿瘤免疫的化合物,并通过中医综合信息数据库预测相关靶点。同时,将结果与 MalaCards 和 CTD 数据库中包含的肺腺癌靶点相关联,从而构建化合物 - 靶点作用网络图,并探索 SD 治疗肺腺癌的机制。在体外实验中,测定细胞活力并使用蛋白质免疫印迹法检测作用靶点的相关表达,以确定 SD 的治疗效果。在本实验中,在 SD 中鉴定出 335 种化学成分,其中 107 种成分与肿瘤免疫相关。经 ADME 筛选后,发现有 11 种化合物可能被人体吸入并影响肺腺癌的生长。体外实验表明,SD 可抑制肺腺癌 A549 细胞的生长。SD 可降低 PCNA 的表达(<0.05),并显著增加 Caspase - 3 的表达(<0.05)。进一步实验结果表明,SD 可显著降低 EGFR 的磷酸化水平(<0.05),SD 还可有效抑制 JAK 和 STAT3 磷酸化的表达(<0.01)并抑制 PI3K 和 AKT 磷酸化的表达(<0.01)。SD 可抑制肺腺癌 A549 细胞的生长,其潜在机制被发现是抑制 EGFR/JAK/STAT3 和 EGFR/PI3K/AKT 信号通路,并且 SD 发挥抗肿瘤作用的物质基础可能是儿茶素、紫杉叶素、甜菜碱、表没食子儿茶素没食子酸酯、芥酸酰胺、鸟苷、山奈酚、羊毛甾醇、桑色素、齐墩果酸和槲皮素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/8858071/771c1ae077e6/ECAM2022-5242179.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/8858071/96dd15b7f44e/ECAM2022-5242179.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/8858071/1c9f50f86ee3/ECAM2022-5242179.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/8858071/3be4eda52f1d/ECAM2022-5242179.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/8858071/cb56eee0c1e5/ECAM2022-5242179.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/8858071/abbd11b2ef7b/ECAM2022-5242179.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/8858071/771c1ae077e6/ECAM2022-5242179.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/8858071/96dd15b7f44e/ECAM2022-5242179.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/8858071/1c9f50f86ee3/ECAM2022-5242179.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/8858071/3be4eda52f1d/ECAM2022-5242179.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/8858071/cb56eee0c1e5/ECAM2022-5242179.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/8858071/abbd11b2ef7b/ECAM2022-5242179.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d74/8858071/771c1ae077e6/ECAM2022-5242179.006.jpg

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