Identification of molecular mechanism of the anti-lung cancer effect of Jin Ning Fang using network pharmacology and its experimental verification

A549 cells were treated with JNF for 48 h. CCK-8 assay showed that cell viability in JNF was significantly lower than in the control group (100.00 ± 1.47 vs. 82.59 ± 2.81, P &lt; 0.01), suggesting that JNF observably inhibited the proliferation of lung cancer cells. Meanwhile, JNF increased the apoptosis rate in A549 cells compared to that in the control group (0.74 ± 0.03 vs. 2.20 ± 0.14, P &lt; 0.01), indicating that JNF treatment may induce apoptosis in lung cancer cells. Next, the expression level of hub genes identified from pharmacological network was detedcted by qPCR analysis. Result showed that JNF could significantly decrease the expression level of <i>FDPS</i>, <i>PIM1</i>, <i>VCAM1</i>, <i>SLC29A1</i>, <i>NQO1</i>, and <i>ESR1</i> (all P &lt; 0.05), while JNF markedly increased the mRNA levels of <i>AR</i> and <i>ANPEP</i> (all P &lt; 0.05).

将A549细胞用JNF处理48小时。采用CCK-8细胞活力检测法检测发现，JNF处理组的细胞活力显著低于对照组（100.00 ± 1.47 vs 82.59 ± 2.81，P < 0.01），提示JNF可显著抑制肺癌细胞的增殖。与此同时，与对照组相比，JNF处理组A549细胞的凋亡率显著升高（0.74 ± 0.03 vs 2.20 ± 0.14，P < 0.01），表明JNF处理可诱导肺癌细胞发生凋亡。随后，通过实时荧光定量聚合酶链式反应（qPCR）分析，对从药理网络中鉴定得到的枢纽基因（hub gene）的表达水平进行检测，结果显示JNF可显著下调FDPS、PIM1、VCAM1、SLC29A1、NQO1及ESR1的表达水平（所有P < 0.05），同时可显著上调AR与ANPEP的mRNA表达水平（所有P < 0.05）。