Arctigenin is a phenylpropanoid metabolite with antioxidant and anti-inflammatory activities. Arctigenin at 1μM inhibited LPS-induced nuclear NF-κB activation and nuclear translocation of p65, accompanied by inhibition of I-κBα phosphorylation. It inhibited LPS-inducible increase in the iNOS mRNA by 0.01–1μM Arctigenin, with IC50 value<0.01μM for inhibition of the induction of iNOS by LPS[8]. Arctigenin also works as an active adiponectin receptor 1 agonist with IC50 value of 2.6μM for AdipoR1[9]. Arctigenin exerted significant neuroprotective effects on glutamate-injured primary cultures of rat cortical cells by directly binding to kainic acid receptors and partly scavenging of free radicals[10].
Arctigenin/牛蒡苷元 细胞实验
Cell Line
Concentration
Treated Time
Description
References
THP-1 cells
20 μM
4 hours
To study the effect of INF39 on inflammation in THP-1 cells, results showed that INF39 enhanced the anti-inflammatory effects of Arctigenin
Am J Transl Res. 2019 Jul 15;11(7):3992-4009
INS-1 β cells
2.5, 5 μM
24 h
ATG significantly prevented palmitate-induced INS-1 β-cell death
Acta Pharmacol Sin. 2012 Jul;33(7):941-52.
HepG2 cells
1, 5, 10 μM
24 h
ATG decreased GFP protein level in a dose-dependent manner, inhibiting protein synthesis
Acta Pharmacol Sin. 2012 Jul;33(7):941-52.
HepG2 cells
5 μM
6 h
ATG significantly inhibited BFA-induced XBP-1 mRNA splicing and eIF2α phosphorylation
ATG inhibited BFA-induced cell death and UPR in a concentration-dependent manner
Acta Pharmacol Sin. 2012 Jul;33(7):941-52.
murine RAW264.7 cells
100, 30, 10 μM
3 h
reduced LPS-induced TNF-α and IL-6 production, downregulated iNOS and COX-2 expression, and decreased NO accumulation
J Adv Res. 2021 Mar 4;33:241-251.
human peripheral blood mononuclear cells (PBMCs)
35.18 ± 6.01 μM
inhibited LPS-induced TNF-α production
J Adv Res. 2021 Mar 4;33:241-251.
Primary microglia
5 or 10 μM
36 h
To investigate the effects of Arctigenin on HMGB1 or TNF-α-stimulated microglial activation and inflammatory responses. Results showed that Arctigenin significantly inhibited the increased expression of Iba-1, TNF-α, IL-1β, and iNOS induced by HMGB1 or TNF-α, and ameliorated morphological changes in microglia.
Br J Pharmacol. 2020 Nov;177(22):5224-5245.
Podocytes
10 μM
24 h
ATG improves podocyte morphology and adhesion under high glucose conditions
Nat Commun. 2019 Oct 4;10(1):4523.
HEK293T cells
10 μM
2 h
ATG binds to PP2A and enhances its activity
Nat Commun. 2019 Oct 4;10(1):4523.
Arctigenin/牛蒡苷元 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
BALB/c mice
IMQ-induced psoriasis model
Topical application
5%
Once daily for 7 consecutive days
Alleviated psoriatic skin inflammation, reduced epidermal thickening and immune cell infiltration, ameliorated splenomegaly, and decreased inflammatory cytokine levels
J Adv Res. 2021 Mar 4;33:241-251.
C57BL/6 mice
Chronic unpredictable mild stress (CUMS)-induced depression model
Oral
25, 50, or 100 mg/kg
Once daily for 6 weeks
To evaluate the antidepressant effects of Arctigenin on CUMS-induced depressive-like behaviors. Results demonstrated that Arctigenin significantly reduced depressive-like behaviors, inhibited microglial activation and neuroinflammatory responses, and acted through the HMGB1/TLR4/NF-κB and TNF-α/TNFR1/NF-κB signaling pathways.
Br J Pharmacol. 2020 Nov;177(22):5224-5245.
Mice
Type 1 and type 2 diabetes models
Oral gavage
40 mg/kg
Once daily for 8 weeks
ATG attenuates proteinuria and podocyte injury
Nat Commun. 2019 Oct 4;10(1):4523.
Mice
Experimental Autoimmune Encephalomyelitis (EAE) model
Intraperitoneal injection
10 mg/kg
Daily administration starting from the first day after EAE induction
Arctigenin treatment delayed the onset of clinical symptoms in EAE mice and significantly reduced cumulative and maximum clinical scores, indicating that arctigenin alleviates clinical symptoms in EAE mice.
Front Immunol. 2021 Jul 19;12:691590
Mice
SOD1G93A transgenic mice
Oral
33.3 mg/kg
Once daily for 6 weeks
A-1 treatment improved motor performance in SOD1G93A mice, reduced skeletal muscle atrophy and fibrosis, mitigated the loss of spinal motor neurons, and decreased glial activation. Additionally, A-1 treatment improved mitochondrial function, as evidenced by elevated ATP levels and increased expression of key mitochondrial-related proteins. The A-1 treatment group also showed decreased levels of IL-1β, pIκBα/IκBα, and pNF-κB/NF-κB.
CNS Neurosci Ther. 2024 Jun;30(6):e14692
Female Balb/c mice
Concanavalin A-induced autoimmune hepatitis model
Intragastric
2.5, 5, and 10 mg/kg
Twice per day for 10 days
Arctigenin pretreatment significantly alleviated the liver injury, as evidenced by biochemical and histopathological investigations, whose protective effects were comparable with Prednisone acetate and Cyclosporin A.
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