Skip to main content

Table 2 TOP 20 significantly different metabolites

From: Comparative analysis of metabolites and in vitro hypoglycemic activity of Taiwanofungus camphoratus cultured using various methods

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

[29,30,31,32]

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

[41, 42]

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

[44, 45]

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

[45,46,47,48]

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

[49,50,51]

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

[52,53,54]

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

[55,56,57,58,59]