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

Table 1

Summary of anti-inflammation experiments of five psoralea prenylflavonoids.

Cells or animals	Model method	Active ingredient	Dosage	Pharmacological effect	Reference number
BV-2 microglia	LPS	Isobavachalcone	2, 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 cells	MALP-2; LPS; Poly[I:C]	Isobavachalcone	20, 50, 100 μmol/L	(i) Inhibited iNOS expression in luciferase reporter and protein level induced by TLRs agonists and inhibited nitrite production	[16]
Microglial cells	LPS	Bavachinin; 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 cells	MALP-2; LPS; Poly[I:C]	Isobavachalcone	0.1, 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]
Chondrocytes	5 ng/ml IL-1β	Bavachin	1, 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 chondrocytes	Non	Bavachin	5, 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 macrophages	LPS	Bavachin	10, 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 macrophages	LPS + IFN-γ	Neobavaisoflavone	2.5, 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 cells	IL-6	Bavachin; 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 mice	Ischemic stroke	4’-O-methybavachalcone	5, 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]