Objective： To screen the key genes of Glioma Decoction-1 （GD-1） in combination with temozolomide （TMZ） against glioma by transcriptomics study.,Methods,2,A subcutaneous glioma heterotopic model was established in mice， and after successful modeling， the mice were grouped for administration， and the tumor volume was measured every third day. Samples were taken after 14 days， and the pathological histomorphology of tumors was observed by HE staining. The potential mechanism of GD-1 combined with TMZ against glioma was predicted by transcriptomics and literature review.,Results,2,Compared with the control group， the average tumor volume of nude mice in the TMZ and TMZ-GD-1 groups was significantly reduced （,P,<,0.05）， and compared with the TMZ group， the tumor volume of the TMZ-GD-1 group was reduced， but the difference was not statistically significant （,P,>,0.05）.He staining showed the highest growth density of glioblastoma in the control group with the largest and hyperchromatic nuclei， and compared with the TMZ group， the TMZ-GD-1 group showed lower growth density of glioblastoma with lighter nuclei and more nuclei emerged pyknosis and lysis. By transcriptomics study， 65 differential genes were found in the GD-1 combined with TMZ group compared with the TMZ group， including 36 up-regulated genes and 29 down-regulated genes. Through GO enrichment analysis and KEGG enrichment analysis， the differential genes related to differentiation， apoptosis and biological signaling transmission during cell development were ,SLC17A7,，, CACNA1D,，, MTCP1,，, RASIP1,，, BTBD16,， among which ,CACNA1D, was down-regulated in MAPK signaling pathway， ,MTCP1, was down-regulated in PI3K/Akt signaling pathway， and ,CACNA1D, was down-regulated in the cGMP/PKG signaling pathway.,Conclusion,2,GD-1 combined with TMZ has better effect in the treatment of glioma than the Western medicine TMZ alone， which could further reduce the tumor volume and lower tumor growth density. The mechanism may be up-regulation of inhibitory oncogenes （SLC17A7， RASIP1， BTBD16） and down-regulation of oncogenes （MTCP1， CACNA1D）， which further affects the activity of PI3K/Akt， cGMP/PKG， MAPK signaling pathways， thereby inhibiting glioma growth.