Taraxasterol inhibits the nuclear factor‑kappa B (NF‑κB) signaling pathway by preventing LPS‑induced NF‑κB translocation from the cytoplasm to the nucleus. [1]
Taraxasterol down‑regulates the expressions of toll‑like receptor 2 (TLR2), TLR4, and NF‑κB p65, and decreases the expression ratio of Bax/Bcl‑2 in hepatic tissues. [2]
Taraxasterol activates liver X receptor α (LXRα) and suppresses LPS‑induced NF‑κB activation. It also inhibits iNOS, COX‑2, VCAM‑1, and ICAM‑1 expression. [3]
Taraxasterol inhibits the phosphorylation of IκB‑α, p65 NF‑κB, p46‑p54 JNK, p42‑p44 ERK, and p38, thereby blocking NF‑κB and MAPK signaling pathways. [4]

In LPS‑induced RAW 264.7 murine macrophages, taraxasterol (2.5, 5, or 12.5 µg/ml) pretreatment for 1 h dose‑dependently inhibited the production of nitric oxide (NO) (p<0.05 or 0.01), prostaglandin E2 (PGE2) (p<0.01 at 5 and 12.5 µg/ml), tumor necrosis factor‑α (TNF‑α), interleukin‑1β (IL‑1β), and interleukin‑6 (IL‑6) (p<0.05 or 0.01). Immunocytochemical analysis showed that taraxasterol prevented LPS‑induced NF‑κB p65 translocation from cytoplasm to nucleus. [1]
In LPS‑stimulated RAW 264.7 cells, taraxasterol at 2.5, 5, and 12.5 µg/ml had no cytotoxic effect (MTT assay). It dose‑dependently reduced NO and PGE2 production, and decreased TNF‑α, IL‑1β, and IL‑6 levels. [1]
In LPS‑stimulated human umbilical vein endothelial cells (HUVECs), taraxasterol (5, 10, 15 µg/ml) had no cytotoxicity up to 15 µg/ml (18 µg/ml decreased viability). It concentration‑dependently reduced TNF‑α, IL‑8, PGE2, and NO production. Western blot showed that taraxasterol reduced iNOS, COX‑2, VCAM‑1, ICAM‑1, and NF‑κB activation, and increased LXRα expression. The inhibition of TNF‑α, IL‑8, PGE2, and NO by taraxasterol was reversed by the LXRα inhibitor geranylgeranyl diphosphate (GGPP, 20 µM). [3]

In a Con A‑induced acute hepatic injury mouse model, taraxasterol (oral administration at 10, 5, 2.5 mg/kg once daily for 7 d) dose‑dependently decreased liver index (significant at 10 mg/kg, p<0.01), serum ALT and AST levels (p<0.01 or p<0.05 at 10 and 5 mg/kg), hepatic MDA levels, and increased hepatic GSH and SOD production. It also inhibited serum TNF‑α, IL‑6, IL‑1β, IFN‑γ, and IL‑4 release. Histological analysis showed reduced inflammatory cell infiltration and necrosis, and TUNEL staining revealed reduced hepatocyte apoptosis. Western blot showed down‑regulation of hepatic TLR2, TLR4, NF‑κB p65, and decreased Bax/Bcl‑2 ratio. [2]
In LPS‑induced acute lung injury (ALI) mice, taraxasterol (intraperitoneal injection at 2.5, 5, 10 mg/kg 1 h before intranasal LPS) dose‑dependently reduced lung wet/dry ratio, MPO activity, total cells, neutrophils, and macrophages in BALF, and decreased BALF and serum levels of TNF‑α, IL‑1β, IL‑6, NO, COX‑2, and PGE2. Histopathology showed attenuated lung injury. Western blot showed inhibition of IκB‑α, p65 NF‑κB, p38, JNK, and ERK phosphorylation. In a survival study, taraxasterol (2.5, 5, 10 mg/kg i.p. 1 h before LPS 20 mg/kg i.p.) gave 26%, 58%, and 78% protection over 7 d, respectively (p<0.05 or p<0.01). [4]

Cell viability was determined by MTT assay. RAW 264.7 cells (4×10⁵ cells/ml) were plated in 96‑well plates, treated with taraxasterol (0‑12.5 µg/ml) for 2 h, then stimulated with LPS (1 µg/ml) for 18 h. MTT (50 µl) was added for 4 h, then removed and cells lysed with DMSO (100 µl/well). Optical density measured at 570 nm. [1]
NO production was measured by Griess reaction. RAW 264.7 cells (4×10⁵ cells/ml) in 24‑well plates were pretreated with taraxasterol (2.5, 5, 12.5 µg/ml) for 1 h, then stimulated with LPS (1 µg/ml) for 24 h. Supernatants were mixed with equal volume of Griess reagent, incubated 15 min at room temperature, and absorbance read at 540 nm. Nitrite concentration determined from sodium nitrite standard curve. [1]
PGE2 and cytokines (TNF‑α, IL‑1β, IL‑6) were measured by ELISA. For PGE2 and NO, cells treated as above (24 h LPS). For cytokines, cells pretreated with taraxasterol for 1 h then stimulated with LPS for 6 h; supernatants collected and assayed per kit instructions. [1]
Immunocytochemical analysis of NF‑κB: RAW 264.7 cells on glass coverslips in 24‑well plates were pretreated with taraxasterol (2.5, 5, 12.5 µg/ml) for 1 h, then stimulated with LPS (1 µg/ml) for 1 h. Cells were fixed with 4% formaldehyde for 30 min, permeabilized with 3% Triton X‑100 for 10 min, blocked with 5% BSA in PBS for 30 min, then incubated with rabbit anti‑NF‑κB/p65 polyclonal antibody, followed by Cy3‑conjugated anti‑rabbit IgG and DAPI staining. Fluorescent signals were analyzed by fluorescence microscopy. [1]
For HUVECs, cell viability was measured by MTT. Cells in 96‑well plates were incubated with taraxasterol for 1 h then stimulated with LPS for 18 h, then MTT added for 3 h, and DMSO (150 µl/well) added to dissolve formazan. [3]
ELISA for TNF‑α and IL‑8: HUVECs pretreated with taraxasterol for 1 h, then LPS for 24 h; supernatants collected and analyzed by ELISA kits. [3]
NO assay in HUVECs: same treatment as above, then supernatant nitrite level measured using Griess reagent. [3]
Western blot for HUVECs: whole cell proteins extracted with RIPA buffer containing protease inhibitor cocktail; 40 µg protein separated on 12% SDS‑PAGE, transferred to PVDF membranes, incubated with primary antibodies against VCAM‑1, ICAM‑1, iNOS, COX‑2, NF‑κB, LXRα, then HRP‑conjugated secondary antibodies, and visualized with chemiluminescence detection kit. [3]

For Con A‑induced acute hepatic injury: Male ICR mice (18‑22 g) were randomly divided into 6 groups (n=10 each). Taraxasterol was orally administered at 10, 5, or 2.5 mg/kg in 0.5% carboxymethyl cellulose sodium (CMC‑Na) once daily for 7 d. Bifendate (200 mg/kg) was used as positive control. Normal and Con A groups received equal volume of 0.5% CMC‑Na. On day 7, 1 h after last administration, mice were injected with a single dose of Con A (18 mg/kg) via tail vein except normal group. After 8 h, blood was collected from retro‑orbital plexus, mice were euthanized by cervical dislocation, and hepatic tissues were collected. [2]
For LPS‑induced acute lung injury and survival: Male BALB/c mice (18‑20 g). For survival, mice were injected i.p. with LPS (20 mg/kg). Taraxasterol (2.5, 5, 10 mg/kg in PBS) was given i.p. 1 h before LPS challenge. Survival was monitored every 12 h for 7 d. For ALI, mice were randomly divided into 7 groups: control, taraxasterol (10 mg/kg) alone, LPS, taraxasterol (2.5, 5, 10 mg/kg)+LPS, and dexamethasone (0.5 mg/kg)+LPS. Taraxasterol was given i.p. in 50 µl PBS 1 h before intranasal instillation of LPS (10 µg in 50 µl PBS). Control mice received PBS i.n. After 7 h, BALF was collected by tracheal cannula with PBS (total 1.3 ml). Lungs were removed for wet/dry ratio, MPO, histology, and Western blot. In a separate experiment, taraxasterol was administered i.p. 1 h after LPS instillation to assess therapeutic effect. [4]

[1]. Effects of taraxasterol on inflammatory responses in lipopolysaccharide-induced RAW 264.7 macrophages. J Ethnopharmacol. 2012 May 7;141(1):206-11.

[2]. Sang R, Yu Y, Ge B, Xu L, Wang Z, Zhang X. Taraxasterol from Taraxacum prevents concanavalin A-induced acute hepatic injury in mice via modulating TLRs/NF-κB and Bax/Bc1-2 signalling pathways. Artif Cells Nanomed Biotechnol. 2019;47(1):3929-3937.

[3]. Anti-inflammatory effects of taraxasterol on LPS-stimulated human umbilical vein endothelial cells. Inflammation, 2018, 41: 1755-1761.

[4]. Protective effect of taraxasterol on acute lung injury induced by lipopolysaccharide in mice. International Immunopharmacology, 2014, 19(2): 342-350.

Dandelionin has been reported to exist in Japanese sea squirts (Balanophora japonica), Palestinian sea squirts (Cota palaestina), and other organisms with relevant data. See also: dandelion sterol (note moved to).

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Taraxasterol inhibits LPS‑induced inflammatory responses in macrophages by blocking the NF‑κB pathway, suggesting its potential as a therapeutic agent for inflammation‑mediated diseases. [1]
Taraxasterol prevents Con A‑induced acute hepatic injury by inhibiting TLRs/NF‑κB inflammatory signaling and promoting Bax/Bcl‑2 anti‑apoptotic signaling, supporting its potential application in immune‑mediated hepatic injury. [2]
Taraxasterol inhibits vascular inflammation in HUVECs by activating LXRα, which subsequently inhibits LPS‑induced NF‑κB activation, and may be a potential anti‑inflammatory agent for cardiovascular diseases. [3]
Taraxasterol protects against LPS‑induced acute lung injury in mice by suppressing NF‑κB and MAPK activation, leading to reduced pro‑inflammatory cytokine expression, and may be a potential agent for prevention and treatment of acute lung injury. [4]

C30H50O

426.7174

426.386

1059-14-9

610148

White to off-white solid powder

1.0±0.1 g/cm3

488.2±14.0 °C at 760 mmHg

221-222°

217.0±12.4 °C

0.0±2.8 mmHg at 25°C

1.534

11.06

1

1

0

31

766

0

XWMMEBCFHUKHEX-UHFFFAOYSA-N

InChI=1S/C30H50O/c1-19-11-14-27(5)17-18-29(7)21(25(27)20(19)2)9-10-23-28(6)15-13-24(31)26(3,4)22(28)12-16-30(23,29)8/h20-25,31H,1,9-18H2,2-8H3

4,4,6a,6b,8a,12,14b-heptamethyl-11-methylidene-1,2,3,4a,5,6,6a,7,8,9,10,12,12a,13,14,14a-hexadecahydropicen-3-ol

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Ethanol : ~5.5 mg/mL (~12.89 mM )
DMSO : ~1 mg/mL (~2.34 mM)

Solubility in Formulation 1: ≥ 0.55 mg/mL (1.29 mM) (saturation unknown) in 10% EtOH + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 5.5 mg/mL clear EtOH stock solution to 400 μL of PEG300 and mix evenly; then add 50 μL of Tween-80 to the above solution and mix evenly; then add 450 μL of normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 0.55 mg/mL (1.29 mM) (saturation unknown) in 10% EtOH + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 5.5 mg/mL clear EtOH stock solution to 900 μL of corn oil and mix well.

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 (Please use freshly prepared in vivo formulations for optimal results.)