Psoralidin is a dual inhibitor of COX-2 and 5-LOX, regulates ionizing radiation (IR)-induced pulmonary inflammation, with anti-cancer, anti-bacterial, and anti-inflammatory properties[3]. Three breast cancer cell populations (ALDH- cells, ALDH+ cells, and commercial BSCSs) are sensitive to Psoralidin treatment (10, 15, 20, and 25 μM; 24 hours) with IC50s ranging from 18 to 21 μM; however, the MCF-12A cells were resistant to Psoralidin. Psoralidin (30 μM; 24 hours) results in a significant induction of apoptosis for ALDH- cells, ALDH+ cells, and commercial BCSCs[4]. Psoralidin decreased the viability of the liver cancer HepG2 cells and exhibited an IC50 of 9 µM. Also, Psoralidin exerted very low toxic effects on the normal AML12 hepatocytes exhibiting an IC50 of 100 µM[5]. Psoralidin treatment could reverse the caffeine-induced dysfunctions and aberrant differentiation of BMSCs (bone marrow mesenchymal stem cells) via the ER pathway[6].
psoralidin/补骨脂定 细胞实验
Cell Line
Concentration
Treated Time
Description
References
PC-3 cells
60 µM
24 hours
Psoralidin inhibited viability and induced apoptosis in PC-3 cells
Apoptosis. 2010 Feb;15(2):153-61
HL-1 cardiomyocytes
10, 20, 50, 100 µM
24 hours
Evaluate the toxic effects of psoralidin on HL-1 cardiomyocytes, showing no significant toxicity at concentrations ≤50 μM.
J Adv Res. 2022 Sep;40:249-261
Commercial breast cancer stem cells (BCSCs)
10, 15, 20, 25 µM
24 hours
To evaluate the effect of psoralidin on cell viability, results showed that psoralidin significantly inhibited the growth of BCSCs with IC50 values ranging from 18-21 μM
Br J Cancer. 2013 Nov 12;109(10):2587-96
MDA-MB-231 cells (ALDH+)
10, 15, 20, 25 µM
24 hours
To evaluate the effect of psoralidin on cell viability, results showed that psoralidin significantly inhibited the growth of ALDH+ cells with IC50 values ranging from 18-21 μM
Br J Cancer. 2013 Nov 12;109(10):2587-96
MDA-MB-231 cells (ALDH-/C0)
10, 15, 20, 25 µM
24 hours
To evaluate the effect of psoralidin on cell viability, results showed that psoralidin significantly inhibited the growth of ALDH-/C0 cells with IC50 values ranging from 18-21 μM
Br J Cancer. 2013 Nov 12;109(10):2587-96
DU-145 cells
45 µM
24 hours
Psoralidin inhibited viability and induced apoptosis in DU-145 cells
Apoptosis. 2010 Feb;15(2):153-61
MG63 cells
0–50 µM
24 or 48 hours
PSO inhibited OS cell proliferation in a dose-dependent and time-dependent manner.
Chin Med. 2023 Mar 31;18(1):34
143B cells
0–50 µM
24 or 48 hours
PSO inhibited OS cell proliferation in a dose-dependent and time-dependent manner.
Psoralidin inhibited both constitutive and epidermal growth factor (EGF)-induced EGFR activation and simultaneously triggered SAPK signaling, resulting in the induction of apoptosis in AIPC cells.
Mol Cancer Ther. 2010 Sep;9(9):2488-96
PC-3 cells
60 µM
30 and 60 minutes
Psoralidin inhibited both constitutive and epidermal growth factor (EGF)-induced EGFR activation and simultaneously triggered SAPK signaling, resulting in the induction of apoptosis in AIPC cells.
Mol Cancer Ther. 2010 Sep;9(9):2488-96
Ichthyophthirius multifiliis theronts
0.8 mg/L or higher
4 hours
Evaluate the killing effect of psoralidin on I. multifiliis theronts, results showed that at 0.8 mg/L or higher concentrations, all theronts were killed within 4 hours
Int J Parasitol Drugs Drug Resist. 2015 Apr 21;5(2):58-64
To evaluate the cytotoxicity of psoralidin and its nanoformulation on A549 cells. Results showed that Ps-CS/BLs had an IC50 value of 3.56 ± 0.36 µg/mL, significantly lower than free psoralidin (48.94 ± 1.3 µg/mL).
To evaluate the cytotoxicity of psoralidin and its nanoformulation on MCF-7 cells. Results showed that Ps-CS/BLs had an IC50 value of 1.19 ± 0.24 µg/mL, significantly lower than free psoralidin (39.85 ± 1.1 µg/mL).
Polymers (Basel). 2023 Mar 15;15(6):1464
HeLa cells
20-50 µM
48 hours
To evaluate the cytotoxic and apoptotic activities of psoralidin in HeLa cells. Results showed that psoralidin induced apoptosis in a concentration-dependent manner, with 13.5 ± 1.2% apoptosis at 50 μM.
Molecules. 2012 May 29;17(6):6449-64
psoralidin/补骨脂定 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
BALB/c mice
ADR-induced cardiotoxicity model
Intraperitoneal injection
12.5, 25, 50 mg/kg
Every two days, three times in total
Psoralidin significantly increased the survival rate of ADR-injured mice, improved cardiac function indicators, and reduced myocardial fibrosis, oxidative stress, and apoptosis.
J Adv Res. 2022 Sep;40:249-261
Goldfish (Carassius auratus)
I. multifiliis infection model
Water bath administration
2.5 mg/L
5 hours
Evaluate the in vivo therapeutic effect of psoralidin on I. multi?liis infected gold?sh, results showed that 2.5 mg/L concentration for 5 hours significantly reduced the number of theronts released
Int J Parasitol Drugs Drug Resist. 2015 Apr 21;5(2):58-64
Balb/c nude mice
CTPE xenograft model
Oral
20 mg/kg
5 days per week for 4-5 weeks
Oral administration of Psoralidin significantly suppressed CTPE xenograft growth without observable toxicity. Tumours from Pso-treated animals showed decreased autophagic morphology, mesenchymal markers expression, and increased epithelial protein expression.
Br J Cancer. 2017 Jun 27;117(1):56-64
Balb/c athymic nude mice
ALDH+, CD44+/CD22− and ALDH− xenograft models
Oral
25 mg/kg
5 days a week for 4 weeks
Psoralidin significantly inhibited the growth of ALDH+, CD44+/CD22? and ALDH? tumors and inhibited Notch-1 mediated EMT activation.
Mol Carcinog. 2017 Mar;56(3):1127-1136
BALB/c nude mice
Orthotopic osteosarcoma mouse model
Oral gavage
5, 10, or 20 mg/kg
Every two days for three weeks
PSO significantly inhibited osteosarcoma growth and metastasis.
Chin Med. 2023 Mar 31;18(1):34
Mice
PC-3 xenograft model
Oral
50 mg/kg
Not specified
Psoralidin inhibited tumor growth and induced apoptosis
Apoptosis. 2010 Feb;15(2):153-61
Nude mice
PC-3 xenograft model
Oral
50 mg/kg
Five days a week for four weeks
Psoralidin effectively suppressed PC-3 xenograft tumors by inhibiting EGFR-mediated survival signaling with a simultaneous induction of SAPK-mediated apoptotic events.
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