Serial number | Compound | Molecular formula | P-value | VIP | Biological activity and mechanism of action | References |
---|---|---|---|---|---|---|
X153 | 1-Linoleoyl glycerol | C21H38O4 | 2.65E−02 | 1.304089 | Anti-inflammatory: can reduce inflammation caused by apolipoprotein CIII (a small glycoprotein that binds to the surface of certain lipoproteins) | [28] |
X174 | Ethyl linoleate | C20H36O2 | 4.58E−02 | 4.386933 | 1. Treatment of atherosclerotic disease: by inhibiting the progression of plaque in ApoE gene deficient mice, the development of atherosclerosis was slowed down 2. Anti-inflammatory, antibacterial: (1) can be used to treat inflammatory and non-inflammatory acne and seborrheic disease; (2) it can down-regulate the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), thereby reducing the production of nitric oxide (NO) and prostaglandin E2, and achieving anti-inflammatory effects 3. Inhibition of melanin formation: the formation of melanin was inhibited by Akt/GSK3β/β-catenin signaling pathway | |
X167 | Linolenic acid ethyl ester | C20H34O2 | 4.69E−02 | 1.903281 | Pro-fibrosis | [33] |
X179 | Ethyl oleate | C20H38O2 | 4.78E−02 | 1.65851 | Can be used as excellent solvent for steroids and other lipid drugs | [34] |
X184 | β-Sitostenone | C29H48O | 3.12E−05 | 1.618023 | Inhibition of tyrosinase activity | [35] |
X132 | Eleostearic acid | C18H30O2 | 2.96E−09 | 1.105423 | Treatment of breast cancer: it can block the proliferation of breast cancer cells and induce apoptosis through an oxidation-dependent mechanism | [36] |
X186 | Linolenic acid | C18H30O2 | 1.18E−03 | 1.124406 | – | – |
X181 | (22E)-Ergosta-4, 6, 8(14), 22-tetraen-3-one | C28H40O | 1.26E−03 | 2.300434 | Against cancer: neuro-2a, Saos-2, MCF7 and LNCaP-C42 | [37] |
X11 | Syringaldehyde | C9H10O4 | 3.35E−05 | 1.229216 | Anti-inflammatory, anti-oxidation, anti-diabetes | [38] |
X51 | 2,4,5-Trimethoxybenzaldehyde | C10H12O4 | 1.27E−05 | 3.710584 | Inhibition of cyclooxygenase 2 (COX-2) | [39] |
X49 | 1,4-Dimethoxybenzene | C8H10O2 | 2.72E−05 | 5.483619 | Attract bees and other insects to complete plant pollination | [40] |
X50 | 3-(2-Hydroxyphenyl)propanoic acid | C9H10O3 | 2.03E−05 | 3.133247 | – | – |
X108 | Gamabufotalin | C24H34O5 | 2.21E−02 | 3.260203999 | 1. Anti-cancer: (1) non-small cell lung cancer can significantly inhibit the expression of COX-2 in non-small cell lung cancer cells, and its mechanism is to inhibit IKKβ/NF-κB signaling pathway. (2) Human multiple myeloma: inhibit the growth of human multiple myeloma cells and induce apoptosis, IC50 < 50 nM; (3) osteosarcoma: inhibition of the viability and tumorigenicity of osteosarcoma cells by blocking the TGF-β/periostin/PI3K/AKT signaling pathway 2. Treatment of angiogenesis-related diseases: inhibition of angiogenesis by inhibiting the activation of VEGFR-2 signaling pathway | |
X109 | Methyl 2-methoxyphenylacetate | C10H12O3 | 2.33E−02 | 1.146733678 | One of the compounds for the synthesis of trans-pterocarpin compounds | [43] |
X88 | Camphoratin C | C29H42O6 | 7.26E−07 | 2.385113 | – | – |
X36 | Fraxetin | C10H8O5 | 1.28E−11 | 1.286482 | 1. Anticancer: ovarian cancer, through the inhibition of TLR4/STAT3 signaling pathway to play a therapeutic role in ovarian cancer 2. Antioxidation 3. Anti-inflammatory 4. Antibacterial | |
X68 | Antcin H | C29H42O6 | 1.07E−09 | 1.025206 | 1. Protective liver: (1) by disrupting the binding of p-JNK to the mitochondrial outer membrane scaffold protein (Sab), the self-sustaining activation of the ROS-dependent MAPK cascade is interfered, thereby protecting the liver from damage 2. Anti-cancer: (1) renal cell carcinoma inhibits the invasion of renal cancer cells by inhibiting the FAK-ERK-C/EBP-β/c-Fos-MMP-7 pathway; (2) lymphoma induces apoptosis of lymphoma cell lines by inhibiting LMP1-induced JAK/STAT pathway-related signals | |
X101 | Zhankuic acid B/Antcin I | C29H42O5 | 7.35E−14 | 3.571542 | 1. Anti-inflammatory 2. Cancer: it can effectively regulate the drug efflux transporter P-gp through non-competitive inhibition and reverse the multidrug resistance (MDR) of tumors | |
X70 | Antcin C | C29H42O5 | 7.42E−15 | 1.296406 | 1. Anti-cancer, liver cancer: (1) promote the apoptosis of liver cancer cells by regulating the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathway; (2) protect hepatocytes from oxidative stress and cell death by activating Nrf2/ARE pathway; (2) (s)-antcin C was cytotoxic to Hep G2 and MCF-7 cells with IC50 values of 14.5 and 12.8 μg/mL, respectively 2. Protect cerebral hemorrhage injury: control microglial inflammation through the TLR-4 pathway, thereby protecting cerebral hemorrhage injury | |
X71 | Antcin K | C29H44O6 | 1.96E−15 | 5.708815 | 1. Treatment of liver injury, liver cancer, hepatitis: (1) it has a good potential to reduce the risk of liver cancer metastasis, and can inhibit the metastasis of human liver cancer cells by inhibiting integrin-mediated adhesion, migration and invasion; (2) induce apoptosis mediated by mitochondria and endoplasmic reticulum stress in human hepatocellular carcinoma cells; 3. Protective and therapeutic mechanisms against N-nitrosodiethylamine-induced liver injury and inflammation by directly scavenging ROS activity and up-regulating antioxidant defense mechanisms 2. Treatment of diabetes and hyperlipidemia: (1) it can dose-dependently reduce blood glucose and lipid levels in high-fat diet (HFD) mice and improve glucose tolerance; (2) it can significantly increase the expression level of glucose transporter 4 (GLUT4) in skeletal muscle cell membrane and reduce the level of glucose-6-phosphatase (G6Pase) mRNA in liver, thus reducing blood glucose level. (3) The expression of peroxisome proliferator-activated receptor α (PPARα) was increased, and the mRNA level of hepatic sterol response element binding protein-1c (SREBP-1c) was decreased, which contributed to the decrease of plasma triglyceride, hepatic steatosis and total cholesterol levels 3. Treatment of rheumatoid arthritis (RA): by down-regulating the phospholipase C-γ/protein kinase C-α pathway, the expression of VEGF in rheumatoid arthritis synovial fibroblasts (RASFs) was significantly inhibited and the migration and lumen formation of endothelial progenitor cells (EPC) were improved |