Oxidative Medicine and Cellular Longevity / 2020 / Article / Tab 1

Review Article

Effects and Mechanisms of Five Psoralea Prenylflavonoids on Aging-Related Diseases

Table 1

Summary of anti-inflammation experiments of five psoralea prenylflavonoids.

Cells or animalsModel methodActive ingredientDosagePharmacological effectReference number

BV-2 microgliaLPSIsobavachalcone2, 5, 10 μmol/L(i) Concentration-dependent inhibitory effects on NO and PGE2 production with an IC50 for inhibiting NO production:
(ii) Blocked the I-κBα degradation and downregulated NF-κB activity
(iii) Inhibited the iNOS and COX-2 mRNA and protein expression
[14]

RAW264.7 murine monocytic cellsMALP-2;
LPS
Poly[I:C]
Isobavachalcone20, 50, 100 μmol/L(i) Inhibited iNOS expression in luciferase reporter and protein level induced by TLRs agonists and inhibited nitrite production[16]

Microglial cellsLPSBavachinin
Isobavachalcone
Neobavaisoflavone
1, 3, 10, 30, 100 μmol/L(i) Concentration-dependent inhibitory effects on NO production with an IC50: 26 μmol/L (bavachinin), 17 μmol/L (isobavachalcone), 29 μmol/L (neobavaisoflavone)[15]

bEnd.3 murine brain endothelial cellsMALP-2;
LPS
Poly[I:C]
Isobavachalcone0.1, 1, 5 μmol/L(i) Downregulated ICAM-1 mRNA and protein expression
(ii) Suppressed NF-κB activity
(iii) Dose-dependently attenuated the adhesion of monocytes to endothelial cells activated by LPS
[20]

Chondrocytes5 ng/ml IL-1βBavachin1, 2.5, 5, 10, 20 μmol/L(i) Decreased IκBα kinase and NF-κB DNA-binding activity
(ii) Inhibited IL-1β-induced RANTES, MCP-2, MIP1-α, and MIP1-β chemokine production
(iii) Reduced migration of THP-1 monocytic cells
[19]

Primary rat chondrocytesNonBavachin5, 10 μmol/L(i) Upregulated aggrecan and collagen type II expression in a dose-dependent manner
(ii) Inhibited MMP-1/3/13, and ADMATS-4/5 expression, and upregulated TIMP-1/2/3/4 expression
(iii) Inhibited iNOS and COX-2 expression and downregulated NO and PGE2 in a dose-dependent manner
[17]

Murine J774A.1 cells and murine peritoneal macrophagesLPSBavachin10, 20, 30, 40 μmol/L(i) Inhibited iNOS and mPGES-1 expression and downregulated NO and PGE2 in a dose-dependent manner
(ii) Inhibited phosphorylation of JNK 1/2 and ERK 1/2, and downregulated NF-κB activity
(iii) Suppressed production of IL-β and the expression of NLRP3 inflammasome complex
(iv) Inhibited production of NO, IL-6 and IL-12p40 in LPS-stimulated murine peritoneal macrophages
[18]

RAW264.7 macrophagesLPS + IFN-γNeobavaisoflavone2.5, 5, 10, 25, 50 μmol/L(i) Inhibited the production of ROS, RNS, and cytokines: IL-1β, IL-6, IL-12p40, IL-12p70, and TNF-α with ED50: 25.00 μmol/L (NO); 23.11 μmol/L (IL-1β); 5.03 μmol/L (IL-6); 5.23 μmol/L (IL-12p40); 5.26 μmol/L (IL-12p70); 18.80 μmol/L (TNF-α)[21]

Hep3B cellsIL-6Bavachin
Bavachinin
Isobavachalcone
Neobavaisoflavone
10, 30, 60 μmol/L(i) Inhibited STAT3 phosphorylation with an IC50 for STAT3-dependent promoter activity: (bavachin), (bavachinin), (isobavachalcone), (neobavaisoflavone)[22]
Male ICR miceIschemic stroke4’-O-methybavachalcone5, 10, 20 mg/kg, oral gavage after animal modeling, daily(i) Improved the area of cerebral infarction, brain edema, and neurobehavioral indexes 48 hours after MCAO/R
(ii) Lowered active-PARP and cleaved-caspase-3 levels
(iii) Inhibited IL-1β, TNF-α, and IL-6 production in ischemic cerebral homogenate
(iv) Reduced NLRP3/GSDMD-mediated pyroptosis of brain tissue and cells
[43]

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