Naringin Dihydrochalcone is an artificial sweetener derived from naringin. Naringin is a major flavanone glycoside obtained from tomatoes, grapefruits, and many other citrus fruits. Naringin exhibits biological properties such as antioxidant, anti-inflammatory, and antiapoptotic activities. Naringin suppresses NF-κB signaling pathway.

Naringin suppresses NF-κ B signaling pathway activation. Naringenin inhibits high glucose-induced proliferation, inflammatory reaction and oxidative stress injury in HBZY-1 cells^[1]. Naringin inhibits AGS cancer cell proliferation in a dose- and time-dependent manner. Phosphorylation of PI3K and its activated downstream targets p-Akt and p-mTOR are significantly decreased at 2 mM in Naringin-treated AGS cells. Naringin induces autophagic cell death in AGS cells. Naringin activated the autophagy related protein in AGS cells^[2]. Naringin protects PC12 cells from 3-NP neurotoxicity. The lactate dehydrogenase release is decreased upon naringin treatment in 3-NP-induced PC12 cells. Naringin treatment enhances the antioxidant defense by increasing the activities of enzymatic antioxidants and the level of reduced glutathione^[3].

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

Treatment with naringin significantly alleviates renal injury in diabetic rats and increases diabetic rats body weight significantly. Administration of naringin effectively alleviates the collagen deposition and renal interstitial fibrosis in diabetic rats. Treatment with naringin could result in decreased levels of ROS and MDA and increased activities of SOD and GSH-Px^[1]. Oral administration of naringin significantly improves the learning and memory abilities. Naringin significantly enhances insulin signaling pathway^[3].

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

582.55

C₂₇H₃₄O₁₄

18916-17-1

柚皮苷二氢查尔酮；柚皮甙二氢查尔酮；柚皮甙二氢查尔酮

Room temperature in continental US; may vary elsewhere.

DMSO : ≥ 100 mg/mL (171.66 mM)

* “≥” means soluble, but saturation unknown.

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： 10% DMSO    40% PEG300    5% Tween-80    45% saline

  Solubility: ≥ 10 mg/mL (17.17 mM); Clear solution

  此方案可获得 ≥ 10 mg/mL (17.17 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 100.0 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

• 2.

  请依序添加每种溶剂： 10% DMSO    90% corn oil

  Solubility: ≥ 10 mg/mL (17.17 mM); Clear solution

  此方案可获得 ≥ 10 mg/mL (17.17 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 100.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

• 3.

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

  Solubility: ≥ 2.5 mg/mL (4.29 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (4.29 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

• [1]. Chen F, et al. Naringin Alleviates Diabetic Kidney Disease through Inhibiting Oxidative Stress and Inflammatory Reaction. PLoS One. 2015 Nov 30;10(11):e0143868.

  [2]. Raha S, et al. Naringin induces autophagy-mediated growth inhibition by downregulating the PI3K/Akt/mTOR cascade via activation of MAPK pathways in AGS cancer cells. Int J Oncol. 2015 Sep;47(3):1061-9.

  [3]. Kulasekaran G, et al. Neuroprotective efficacy of naringin on 3-nitropropionic acid-induced mitochondrial dysfunction through the modulation of Nrf2 signaling pathway in PC12 cells. Mol Cell Biochem. 2015 Nov;409(1-2):199-211.

  [4]. Wang D, et al. Naringin Improves Neuronal Insulin Signaling, Brain Mitochondrial Function, and Cognitive Function in High-Fat Diet-Induced Obese Mice. Cell Mol Neurobiol. 2015 Oct;35(7):1061-71.

HBZY-1 cells are plated into 96-well plates and pretreated with various concentrations(1, 5, 10, 25, 50, 100 μM) of naringin for 2 h. Then cells are treated with 30 mM glucose for 24 h. The control group is added sterile normal saline in the same volume. After treatment, all the wells are incubated with 20 μl of 5 mg/ml MTT for 4 h at 37°C. Subsequently, 100 μl of DMSO are used to dissolve the formed formazan crystals after removal of the supernatant. The result is recorded at 490 nm on a microplate reader^[1].

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

Rats: The rats are randomly divided into six groups: control, naringin (80 mg/kg), STZ, STZ+naringin (20 mg/kg), STZ+naringin (40 mg/kg), STZ+naringin(80 mg/kg). The rats in the STZ and STZ+naringin groups are intraperitoneally injected with STZ (65 mg/kg). The control and naringin groups are intraperitoneally injected with 0.1 M citrate buffer of same volume. After injection of STZ for 3 and 5 days, blood glucose levels are measured by tail vein puncture blood sampling^[1].

Mice: Sixty 4-week-old male mice are randomized into four groups and fed for 20 weeks with either control diet or high-fat diet chow. Mice are dosed with 100 mg/kg of naringin daily. Mice body weight and food intake are weekly measured. Following behavioral assessment, animals are deeply anesthetized with isoflurane and sacrificed by decapitation after fasting for at least 5 h. Their plasma is collected for further analysis^[4].

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

• [1]. Chen F, et al. Naringin Alleviates Diabetic Kidney Disease through Inhibiting Oxidative Stress and Inflammatory Reaction. PLoS One. 2015 Nov 30;10(11):e0143868.

  [2]. Raha S, et al. Naringin induces autophagy-mediated growth inhibition by downregulating the PI3K/Akt/mTOR cascade via activation of MAPK pathways in AGS cancer cells. Int J Oncol. 2015 Sep;47(3):1061-9.

  [3]. Kulasekaran G, et al. Neuroprotective efficacy of naringin on 3-nitropropionic acid-induced mitochondrial dysfunction through the modulation of Nrf2 signaling pathway in PC12 cells. Mol Cell Biochem. 2015 Nov;409(1-2):199-211.

  [4]. Wang D, et al. Naringin Improves Neuronal Insulin Signaling, Brain Mitochondrial Function, and Cognitive Function in High-Fat Diet-Induced Obese Mice. Cell Mol Neurobiol. 2015 Oct;35(7):1061-71.