肺癌
汤剂
医学
TLR4型
细胞凋亡
体内
脾脏
中医药
癌症
MTT法
活力测定
癌症研究
污渍
肿瘤坏死因子α
H&E染色
传统医学
染色
药理学
病理
免疫学
化学
生物
内科学
炎症
生物化学
基因
生物技术
替代医学
作者
Wenjie Zhao,Liu Zd,Zhenyong Zhang,Zichao Chen,Jinhua Liu,Peng Sun,Yaqun Li,Dongmei Qi,Zhen Zhang
标识
DOI:10.1016/j.jep.2023.116948
摘要
Si Jun Zi decoction (SJZT) is a traditional Chinese medicine (TCM) formula with the effect of invigorating the spleen qi and replenishing qi. TCM believes that a strong spleen qi helps to strengthen lung qi. Lung cancer is often caused by a deficiency of lung qi. Based on this theory, TCM often applies SJZT to the treatment of lung cancer and has achieved remarkable results. However, the mechanism of SJZT in the treatment of lung cancer remains unclear and requires further study. The main purpose of this study is to explore the mechanism of SJZT against lung cancer. In this study, the chemical constituents in SJZT were analyzed by UPLC-Q-Exactive-MS/MS. MTT and cell scratch test were used to determine the cell viability and inhibition of migration in vitro. The effect of SJZT on the expression of PD-L1 protein in A549 cells was detected by Western Blotting (WB). Apoptosis was detected by crystal violet staining. The mouse model of Lewis lung cancer was established in vivo, and the levels of serum TNF-α and IL-2 were detected by enzyme linked immunosorbent assay (ELISA). The protein levels of TLR4, MyD88, NF-κB and PD-L1 in tumor tissues of mice were detected by WB. Quantitative real-time PCR (qRT-PCR) was used to detect the levels of TLR4, MyD88, NF-κB and PD-L1 mRNA. Finally, hematoxylin and eosin (H&E) staining were used to detect the pathological status of tumor tissues in mice. A total of 16 active chemical constituents were identified in SJZT. In vitro experiments showed that SJZT could inhibit the growth of A549, induce apoptosis and reduce the expression of PD-L1. In vivo experiments showed that SJZT regulated TLR4/MyD88/NF-κB signaling pathway, decreased the expression of PD-L1, and inhibited tumor growth. SJZT inhibits the growth of lung cancer by regulating TLR4/MyD88/NF-κB signal pathway and reducing the expression of PD-L1.
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