Troxerutin, also known as vitamin P4, is a tri-hydroxyethylated derivative of natural bioflavonoid rutins which can inhibit the production of reactive oxygen species (ROS) and depress ER stress-mediated NOD activation.

ROS^[1], NOD^[2]

The results reveal that the maximum protective effect against ROS induced cell damage in the HDP cells occurs following pretreatment with 10 μM Troxerutin. Treatment with H₂O₂ alone decreases cell viability to 77.33±2.44%; however, pretreatment with 10 μM Troxerutin maintains cell viability at 90.88±2.24% following H₂O₂ exposure (P<0.05). At concentrations of 5 and 10 μM, pretreatment with Troxerutin causes a decrease in the number of cells in the sub G1 phase, indicative of cell death. In the control and Troxerutin-only-treated cells, 3.58±0.15 and 0.89±0.11% are 2′7′-dichlorofluorescein (DCF)-positive (P<0.05), whereas treatment with H₂O₂ alone increases the level of ROS to 46.36±2.33%. The cells pretreated with Troxerutin are 19.92±1.95% DCF-positive following H₂O₂ treatment, indicating that Troxerutin reduces the H₂O₂-induced production of ROS in the HDP cells^[1] .

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Troxerutin effectively lowers body weight and obesity-related metabolic parameters in high-fat diet (HFD)-treated mice. Oral administration of Troxerutin notably inhibits those liver injuries in HFD-treated mice, restores glucose intolerance and insulin signaling, and diminishes hepatic gluconeogenesis in HFD-treated mice. Troxerutin remarkably inhibits the nuclear translocation of NF-κB p65, as well as the expressions of its target genes, in the livers of HFD-treated mice. Troxerutin also depresses endoplasmic reticulum (ER) stress-mediated Nucleotide oligomerization domain (NOD) activation in HFD-treated mouse livers^[2]. Lipid depositions in tunica intimae and tunica media are attenuated in Troxerutin-treated diabetic rats compare with untreated diabetic rats. Structural disarrangement and deformity of smooth muscle cells in aortic tissue of Troxerutin-treated diabetic rats are considerably lower than histology of untreated diabetic aorta. Administration of Troxerutin for four weeks to diabetic rats significantly reduces the level of malondialdehyde (MDA) compare to that of untreated diabetic rats (P<0.01)^[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

742.68

C₃₃H₄₂O₁₉

7085-55-4

维生素P4；维脑路通；三氧乙基芦丁；曲可芦丁；托克芦丁；曲克芦丁

Room temperature in continental US; may vary elsewhere.

DMSO : 100 mg/mL (134.65 mM; Need ultrasonic and warming)

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂：;0.5% CMC-Na/saline water

  Solubility: 24 mg/mL (32.32 mM); Clear solution; Need ultrasonic
• 2.

  请依序添加每种溶剂：;10% DMSO ;; 40% PEG300 ;; 5% Tween-80 ;; 45% saline

  Solubility: ≥ 2.5 mg/mL (3.37 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (3.37 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

• 3.

  请依序添加每种溶剂：;10% DMSO ;; 90% (20% SBE-β-CD in saline)

  Solubility: ≥ 2.5 mg/mL (3.37 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (3.37 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

  将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
• 4.

  请依序添加每种溶剂：;10% DMSO ;; 90% corn oil

  Solubility: ≥ 2.5 mg/mL (3.37 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (3.37 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

• [1]. Lim KM, et al. Analysis of changes in microRNA expression profiles in response to the troxerutin-mediated antioxidant effect in human dermal papilla cells. Mol Med Rep. 2015 Aug;12(2):2650-60.

  [2]. Zhang Z, et al. Troxerutin Attenuates Enhancement of Hepatic Gluconeogenesis by Inhibiting NOD Activation-Mediated Inflammation in High-Fat Diet-Treated Mice. Int J Mol Sci. 2016 Dec 25;18(1). pii: E31.

  [3]. Badalzadeh R, et al. Beneficial effect of troxerutin on diabetes-induced vascular damages in rat aorta: histopathological alterations and antioxidation mechanism. Int J Endocrinol Metab. 2015 Apr 30;13(2):e25969.

The cells are plated at a density of 4×10³/well in a 96-well plate. At 70 to 80% confluence, the cells are treated with Troxerutin at concentrations ranging between 0 and 60 μM for 24 h at 37°C. Subsequently, 10 μL water soluble tetrazolium salt assay solution is added to each well and, following incubation for 30 min at 37°C, the optical density is measured at 490 nm using a reader. To examine Troxerutin mediated ROS protection, the cells are pretreated with Troxerutin at the following concentrations: 0, 5, 10 and 15 μM for 8 h. Subsequently, 750 μM H₂O₂ is added to each well. Following incubation for 24 h at 37°C, cell viability is evaluated using an Cell Viability Assay kit. The level of cell viability (%) is normalized to that of 0.1% dimethyl-sulfoxide (DMSO)-treated cells. Each experiment is repeated at least three times^[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Thirty two adult male Wistar rats weighing 250 to 300 grams are used in this study. The animals are randomly divided into four groups (n=8/each) as: group I: control (C), group II: control with Troxerutin (C+TXR), group III: diabetic (D), and group IV: diabetic with Troxerutin (D+TXR). The control rats are received the same amount of citrate buffer alone. Development of diabetes is confirmed by measuring blood glucose levels, 72 hours later. Animals with blood glucose levels higher than 16.65 mM (300 mg/dL) are considered diabetic and those with blood glucose levels lower than this value are excluded from the experiment. Troxerutin (150 mg/kg/day) is administered orally, once daily for four weeks. After 10 weeks of induction of diabetes, diabetic animals as well as the time-matched controls are killed and aortic samples are collected^[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

• [1]. Lim KM, et al. Analysis of changes in microRNA expression profiles in response to the troxerutin-mediated antioxidant effect in human dermal papilla cells. Mol Med Rep. 2015 Aug;12(2):2650-60.

  [2]. Zhang Z, et al. Troxerutin Attenuates Enhancement of Hepatic Gluconeogenesis by Inhibiting NOD Activation-Mediated Inflammation in High-Fat Diet-Treated Mice. Int J Mol Sci. 2016 Dec 25;18(1). pii: E31.

  [3]. Badalzadeh R, et al. Beneficial effect of troxerutin on diabetes-induced vascular damages in rat aorta: histopathological alterations and antioxidation mechanism. Int J Endocrinol Metab. 2015 Apr 30;13(2):e25969.