Tectorigenin is an isoflavonoid plant that was first isolated from Pueraria thomsonii Benth's dried flowers. The formation of ROS generated by palmitic acid (PA) may be reduced by treating HUVECs with irisogenin at doses ranging from 0.1 to 10 μM. Irisogenin treatment reduced increased IKKβ phosphorylation and, at doses ranging from 0.1 to 10 μM, significantly inhibited NF-κB activation by p65 phosphorylation. In a concentration-dependent manner, irisogenin therapy also successfully reduced PA-enhanced TNF-α and IL-6 production [1]. Treatment with irisogenin resulted in a concentration- and time-dependent decrease in the number of viable HepG2 cells. HepG2 cells showed survival rates of 91%, 79%, and 62%, respectively, after being treated with 5, 10, and 20 mg/L irisogenin for 24 hours [2].

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In Vitro: Tectorigenin (0.1, 1, 10 μM) dose‑dependently inhibited PA (100 μM, 30 min)-induced reactive oxygen species (ROS) production in human umbilical vein endothelial cells (HUVECs) as measured by DCFH‑DA fluorescence, with potency similar to 1 mM GSH [1].
Tectorigenin (0.1‑10 μM) reversed PA‑induced collapse of mitochondrial membrane potential (ΔΨm) in HUVECs assessed by JC‑1 staining, indicating protection against mitochondrial dysfunction [1].
Tectorigenin (0.1‑10 μM) significantly inhibited PA‑induced phosphorylation of IKKβ (Tyr199) and NF‑κB p65 (Ser536), as well as JNK (Thr183/Tyr185) in HUVECs, as shown by Western blot. Salicylate (5 mM, IKKβ inhibitor) and GSH (1 mM) were used as positive controls [1].
Tectorigenin (0.1‑10 μM) reduced PA‑stimulated secretion of TNF‑α and IL‑6 in HUVECs after 12 h, measured by ELISA. Salicylate (5 mM) also inhibited cytokine production [1].
Tectorigenin (0.1‑10 μM) decreased PA‑induced serine phosphorylation of IRS‑1 (Ser307) and subsequently enhanced insulin (100 nM)-mediated tyrosine phosphorylation of IRS‑1 (detected by PY99 antibody) in HUVECs [1].
Tectorigenin (0.1‑10 μM) restored insulin‑stimulated phosphorylation of Akt (Thr308) and eNOS (Ser1177) in PA‑treated HUVECs, and increased insulin‑induced NO production (DAF‑FM DA fluorescence). Salicylate and GSH showed similar effects [1].
Tectorigenin (0.1‑10 μM) dose‑dependently inhibited PA‑enhanced expression of endothelin‑1 (ET‑1) and vascular cell adhesion molecule‑1 (VCAM‑1) mRNA in HUVECs, as determined by RT‑PCR. The ERK inhibitor PD98059 (20 μM) also reduced ET‑1 and VCAM‑1 expression, whereas the PI3K inhibitor wortmannin (100 nM) further increased insulin‑stimulated ET‑1/VCAM‑1 [1].

Cell Assay: Human umbilical vein endothelial cells (HUVECs) were cultured in RPMI 1640 with 10% FBS, 100 U/ml penicillin, 100 U/ml streptomycin at 37 °C, 5% CO₂. For experiments, cells were serum‑starved for 12 h, then pretreated with Tectorigenin (0.1, 1, 10 μM), salicylate (5 mM), GSH (1 mM), MitoQ (0.1, 1 μM), wortmannin (100 nM), or PD98059 (20 μM) for 30 min, followed by stimulation with PA (100 μM) for 30 min (or 12 h for cytokine measurement). Insulin (100 nM) was added for 20 min (or 5 min for NO) where indicated [1].
ROS measurement: Cells loaded with 10 μM DCFH‑DA for 30 min at 37 °C, washed, fixed, and fluorescence (ex 488 nm/em 525 nm) observed under an Olympus IX81 microscope [1].
Mitochondrial membrane potential: Cells stained with 25 μg/ml JC‑1 for 30 min, washed, fixed, and red fluorescence (ex 585 nm/em 590 nm) observed. CCCP (10 μM, 20 min) was used as positive control for depolarization [1].
Western blot: Cells lysed in RIPA buffer with PMSF. Proteins separated by 10% SDS‑PAGE, transferred to PVDF, blocked with 5% non‑fat milk, probed with primary antibodies (1:800) overnight at 4 °C, then HRP‑conjugated secondary antibodies (1:2000). Signals detected by ECL. Antibodies used: p‑IRS‑1 (Ser307), IRS‑1, PY99 (for Tyr‑phosphorylated IRS‑1), p‑Akt (Thr308), Akt, p‑IKKβ (Tyr199), IKKβ, p‑NF‑κB p65 (Ser536), NF‑κB p65, p‑SAPK/JNK (Thr183/Tyr185), SAPK/JNK, p‑eNOS (Ser1177), eNOS [1].
ELISA for TNF‑α and IL‑6: Culture supernatants collected after 12 h PA stimulation, assayed using commercial kits according to manufacturer’s instructions [1].
RT‑PCR: Total RNA extracted with TRNzol, cDNA synthesized, PCR performed with specific primers for ET‑1, VCAM‑1, and β‑actin. Products run on 1.5% agarose gel with ethidium bromide, visualized under UV, quantified by Quantity One [1].
NO production: Cells loaded with 5 μM DAF‑FM DA for 30 min, washed, then stimulated with insulin (100 nM) for 5 min, fixed, and fluorescence (ex 495 nm/em 515 nm) observed [1].

Animal Protocol: Male Sprague‑Dawley rats (200‑250 g) were sacrificed by cervical dislocation. Thoracic aortas were removed and placed in ice‑cold Krebs‑Henseleit (K‑H) solution (118.3 mM NaCl, 4.7 mM KCl, 1.2 mM MgSO₄, 1.2 mM KH₂PO₄, 2.5 mM CaCl₂, 25 mM NaHCO₃, 0.026 mM EDTA, 5.0 mM glucose, pH 7.4) gassed with 95% O₂/5% CO₂. Aortas were cleaned of connective tissue and cut into rings (5 mm length). Aortic rings were suspended in organ baths containing 30 mL K‑H solution at 37 °C, pH 7.4, continuously aerated. A resting tension of 2.0 g was applied, and changes in tension measured with a force‑displacement transducer. After 1 h equilibration, rings were exposed to 60 mM KCl to assess constriction. Endothelial integrity was confirmed by >80% relaxation to 10⁻⁵ M acetylcholine after pre‑contraction with 10⁻⁶ M phenylephrine. For experiments, rings were pre‑incubated with Tectorigenin (0.1, 1, 10 μM) or salicylate (5 mM) for 30 min, then PA (100 μM) for another 30 min. After washout, rings were pre‑contracted with 10⁻⁶ M phenylephrine, and cumulative concentration‑response curves to insulin (10⁻⁹–10⁻⁶ M) were obtained. Relaxation expressed as percentage of phenylephrine‑induced contraction [1].

[1]. Tectorigenin Attenuates Palmitate-Induced Endothelial Insulin Resistance via Targeting ROS-Associated Inflammation and IRS-1 Pathway. PLoS One. 2013 Jun 19;8(6):e66417.

[2]. Pro-apoptotic effects of tectorigenin on human hepatocellular carcinoma HepG2 cells. World J Gastroenterol. 2012 Apr 21;18(15):1753-64.

Tectorigenin is a methoxyisoflavone with a structure in which the isoflavone is substituted with a methoxy group at the 6' position and hydroxyl groups at the 5', 7', and 4' positions, respectively. It possesses anti-inflammatory activity and is a plant metabolite. Tectorigenin belongs to the 7-hydroxyisoflavones and methoxyisoflavones class of compounds, and its function is related to that of isoflavones. Tectorigenin has been found in plants of the genus Iris (such as Iris tectorum and Iris mioga) and other organisms with relevant data. Tectorigenin is an isoflavone extracted from kudzu root (Pueraria thunbergiana) that can induce differentiation and apoptosis in cancer cells. (National Cancer Institute, USA)

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Additional Info: Tectorigenin is an isoflavonoid isolated from Pueraria thomsonii Benth. (Fen‑ge‑hua). It has previously been reported to have hypoglycemic, aldose reductase inhibitory, anti‑inflammatory, and antioxidant activities. This study demonstrates that Tectorigenin ameliorates palmitate‑induced endothelial insulin resistance by suppressing ROS‑associated inflammation (IKKβ/NF‑κB and JNK pathways) and restoring IRS‑1/PI3K/Akt/eNOS signaling, leading to increased NO production and improved insulin‑mediated vasodilation. It also reduces ET‑1 and VCAM‑1 expression, suggesting a beneficial effect on the balance between vasodilator and vasoconstrictor actions of insulin. These findings indicate potential application of Tectorigenin for cardiovascular diseases associated with diabetes and insulin resistance [1].

300.063

548-77-6

5281811

Light yellow to yellow solid powder

1.512

601.5±55.0 °C at 760 mmHg

225-226°

230.1±25.0 °C

0.0±1.8 mmHg at 25°C

1.697

2.54

3

6

2

22

454

0

O1C([H])=C(C2C([H])=C([H])C(=C([H])C=2[H])O[H])C(C2C(=C(C(=C([H])C1=2)O[H])OC([H])([H])[H])O[H])=O

OBBCRPUNCUPUOS-UHFFFAOYSA-N

InChI=1S/C16H12O6/c1-21-16-11(18)6-12-13(15(16)20)14(19)10(7-22-12)8-2-4-9(17)5-3-8/h2-7,17-18,20H,1H3

5,7-dihydroxy-3-(4-hydroxyphenyl)-6-methoxychromen-4-one

Tectorigenin K251T K 251T

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

DMSO : ~120 mg/mL (~399.65 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (6.93 mM) (saturation unknown) in 10% DMSO + 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 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL 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: ≥ 2.08 mg/mL (6.93 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in 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 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (6.93 mM) (saturation unknown) in 10% DMSO + 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 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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