- Neohesperidin dihydrochalcone acts as an allosteric effector targeting porcine pancreatic alpha-amylase (PPA), functioning as a non-essential activator with maximal activation (up to threefold) at 4.8 mM [2]

新橙皮苷二氢查耳酮以浓度依赖性方式有效清除活性氧（ROS）和稳定自由基。特别是，最有效的 H2O2 和 HOCl 抑制剂是新橙皮苷二氢查尔酮。新橙皮苷二氢查耳酮具有 93.5% HOCl 清除活性和 73.5% H2O2 清除活性。 Neohesperidin dihydrochalcone 的 IC50 值为 205.1 和 25.5 μM，具有广泛的抑制作用，特别是对非自由基 ROS H2O2 和 HOCl [1]。研究发现，新橙皮苷二氢查尔酮的 IC50 为 389 μM，可激活猪胰腺 α-淀粉酶 (PPA) [2]。

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- 新橙皮苷二氢查尔酮对多种活性氧（ROS）和稳定自由基（包括.ABTS+、.O2-、.OH、H2O2和HOCl）具有浓度依赖性清除活性。它对HOCl（清除率93.5%）和H2O2（清除率73.5%）的清除活性最强，优于抗坏血酸和BHT。此外，它能抑制HOCl诱导的质粒DNA链断裂、血清白蛋白降解以及HIT-T15和HUVEC细胞死亡，而甘露醇、BHT和抗坏血酸无法提供有效的保护作用 [1]
- 新橙皮苷二氢查尔酮对猪胰腺α-淀粉酶（PPA）具有激活作用，而非抑制作用（与其他黄酮类化合物不同）。分子对接模拟显示，它与PPA N端的亲水位点结合，远离酶的活性中心。在4.8 mM浓度时，对PPA的最大激活效果高达3倍，α < 1 < beta参数表明其具有高激活特性 [2]

当给予新橙皮苷二氢查尔酮时，两种有助于肝损伤的指标——AST和ALT——的活性显着降低。新橙皮苷二氢查尔酮可以抑制 PQ 治疗小鼠肝脏中 NF-κB、IL-6、IL-1β 和 TNF-α 蛋白的相对量 [3]。在 Wistar Crl:(WI)WU BR 大鼠中研究了新橙皮苷二氢查尔酮的胚胎毒性和致畸性。当饮食水平高达 5%（每天约 3.3 g/kg 体重）时，新橙皮苷二氢查尔酮不会对大鼠造成任何负面影响 [4]。

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- 在百草枯（PQ）诱导的急性肝损伤小鼠模型（单次腹腔注射75 mg/kg体重PQ）中，新橙皮苷二氢查尔酮通过逆转异常指标发挥保护作用。它降低了血清中天冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT）（关键肝损伤生物标志物）的活性，通过提高谷胱甘肽过氧化物酶（GP-X）、谷胱甘肽-S-转移酶（GST）和过氧化氢酶（CAT）的活性，以及谷胱甘肽（GSH）和总抗氧化能力（T-AOC）的水平，恢复了抗氧化能力。它还降低了活性氧（ROS）和硫代巴比妥酸反应性物质（TBARS）的水平，改善了肝组织的病理变化，下调了环氧合酶-2（COX-2）和诱导型一氧化氮合酶（iNOS）的表达，抑制了核因子-κB（NF-κB）的表达和线粒体介导的凋亡信号通路，并减少了PQ诱导的细胞凋亡（经TUNEL assay证实） [3]

- α-淀粉酶激活实验：将猪胰腺α-淀粉酶（PPA）与适宜底物构建反应体系，向体系中加入不同浓度的新橙皮苷二氢查尔酮，检测酶活性以评估激活效果。进一步进行分子对接模拟，预测新橙皮苷二氢查尔酮与PPA的结合位点，分析化合物与酶的相互作用模式 [2]
- 自由基清除活性实验：建立不同活性氧（ROS）和稳定自由基（.ABTS+、.O2-、.OH、H2O2、HOCl）的反应体系，向各体系中分别加入不同浓度的新橙皮苷二氢查尔酮、抗坏血酸和BHT，测定化合物对每种自由基/ROS的清除率，比较其抗氧化能力 [1]

- 细胞活力实验：培养HIT-T15和HUVEC细胞，用HOCl处理诱导细胞死亡，分别向细胞培养物中加入新橙皮苷二氢查尔酮、甘露醇、BHT和抗坏血酸。孵育后检测细胞存活率，评估新橙皮苷二氢查尔酮对HOCl诱导的细胞死亡的保护作用 [1]
- DNA链断裂实验：将质粒DNA与HOCl孵育以诱导链断裂，向反应体系中加入新橙皮苷二氢查尔酮，通过琼脂糖凝胶电泳检测质粒DNA的完整性，评价化合物对HOCl诱导的DNA链断裂的抑制作用 [1]
- 蛋白降解实验：将血清白蛋白与HOCl孵育以诱导降解，向混合物中加入新橙皮苷二氢查尔酮，采用十二烷基硫酸钠-聚丙烯酰胺凝胶电泳（SDS-PAGE）分析血清白蛋白的降解程度，确定化合物对HOCl诱导的蛋白降解的抑制作用 [1]

- Paraquat-induced liver injury model in mice: Male mice were randomly divided into groups. The model group was given a single intraperitoneal injection of paraquat (75 mg/kg body weight) to induce acute liver injury. The treatment groups were administered Neohesperidin dihydrochalcone (specific dosage not specified in the literature) through an appropriate route (not specified in the literature) before or after PQ injection. The control group received normal saline or vehicle. After a certain period of intervention, blood samples were collected to detect serum AST and ALT activities; liver tissues were harvested to measure antioxidant-related indicators (GP-X, GST, CAT, GSH, T-AOC, ROS, TBARS), perform histopathological examination, immunochemical staining for COX-2 and iNOS, and TUNEL assay to evaluate apoptosis [3]
- Embryotoxicity and teratogenicity study in rats: Twenty-eight mated female Wistar Crl:(WI)WU BR rats per group were fed diets containing Neohesperidin dihydrochalcone at concentrations of 0, 1.25%, 2.5%, or 5% from day 0 to 21 of gestation. The intake of Neohesperidin dihydrochalcone in the low-, mid-, and high-dose groups was 0.8-0.9, 1.6-1.7, and 3.1-3.4 g/kg bw/day, respectively. At Cesarean section, the number of pregnant rats, body weights and weight gains of dams, fecundity and gestation index, number of corpora lutea, implantation sites, live/dead fetuses, resorptions, pre- and post-implantation losses, sex ratio, weights of gravid/empty uterus, ovaries, and placenta were recorded. Fetuses were examined for external, visceral, and skeletal changes [4]

- In Wistar rats treated with Neohesperidin dihydrochalcone at dietary concentrations up to 5% (intake of ~3.3 g/kg bw/day) during gestation, no adverse effects were observed. All animals survived, with no significant differences in dam body weights and weight gains compared to the control group. No embryotoxic, fetotoxic, or teratogenic effects were found, as evidenced by normal reproductive parameters and no abnormalities in fetal external, visceral, or skeletal examinations. The only observed change was cecal enlargement, which is a physiological adaptive response to high doses of low-digestible substances and lacks toxicological relevance [4]
- In mice with paraquat-induced liver injury, Neohesperidin dihydrochalcone showed no obvious toxic side effects while exerting protective effects on the liver, as indicated by the restoration of liver function and antioxidant capacity without causing additional pathological changes [3]

[1]. Antioxidant properties of neohesperidin dihydrochalcone: inhibition of hypochlorous acid-induced DNA strand breakage, protein degradation, and cell death. Biol Pharm Bull. 2007 Feb;30(2):324-30.

[2]. Neohesperidin dihydrochalcone: presentation of a small molecule activator of mammalian alpha-amylase as an allosteric effector. FEBS Lett. 2013 Mar 18;587(6):652-8.

[3]. Artificial sweetener neohesperidin dihydrochalcone showed antioxidative, anti-inflammatory and anti-apoptosis effects against paraquat-induced liver injury in mice. Int Immunopharmacol. 2015 Dec;29(2):722-9.

[4]. Embryotoxicity and teratogenicity study with neohesperidin dihydrochalcone in rats. Regul Toxicol Pharmacol. 2004 Aug;40(1):74-9.

Neohesperidin dihydrochalcone appears as off-white crystals or powder. Insoluble in water. (NTP, 1992)
Neohesperidin dihydrochalcone is a member of the dihydrochalcones that is 3,2',4',6'-tetrahydroxy-4-methoxydihydrochalcone attached to a neohesperidosyl residue at position 4' via glycosidic linkage. It is found in sweet orange. It has a role as an environmental contaminant, a xenobiotic, a plant metabolite and a sweetening agent. It is a neohesperidoside, a disaccharide derivative and a member of dihydrochalcones.
Neohesperidin dihydrochalcone has been reported in Citrus reticulata, Vicia faba, and Citrus deliciosa with data available.

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- Neohesperidin dihydrochalcone is a non-nutritive artificial sweetener produced by hydrogenation of neohesperidin [1]
- It is a potent antioxidant and a novel HOCl scavenger, with potential therapeutic effects on ROS-related inflammatory diseases [1]
- Unlike most flavonoids and their precursor trans-chalcone (which are inhibitors of mammalian alpha-amylase), Neohesperidin dihydrochalcone acts as an allosteric activator of porcine pancreatic alpha-amylase [2]
- It exerts antioxidative, anti-inflammatory, and anti-apoptotic effects against paraquat-induced acute liver damage in mice through multiple mechanisms, including regulating antioxidant enzyme activities, inhibiting inflammatory factor expression, and suppressing apoptotic signaling pathways [3]

C₂₈H₃₆O₁₅

612.58

612.205

20702-77-6

Neohesperidin;13241-33-3

30231

White to off-white solid powder

1.6±0.1 g/cm3

927.1±65.0 °C at 760 mmHg

156-158 °C(lit.)

302.6±27.8 °C

0.0±0.3 mmHg at 25°C

1.684

3.09

245.29

9

15

10

43

882

10

C[C@H]1[C@@H]([C@H]([C@H]([C@@H](O1)O[C@@H]2[C@H]([C@@H]([C@H](O[C@H]2OC3=CC(=C(C(=C3)O)C(=O)CCC4=CC(=C(C=C4)OC)O)O)CO)O)O)O)O)O

ITVGXXMINPYUHD-CUVHLRMHSA-N

InChI=1S/C28H36O15/c1-11-21(34)23(36)25(38)27(40-11)43-26-24(37)22(35)19(10-29)42-28(26)41-13-8-16(32)20(17(33)9-13)14(30)5-3-12-4-6-18(39-2)15(31)7-12/h4,6-9,11,19,21-29,31-38H,3,5,10H2,1-2H3/t11-,19+,21-,22+,23+,24-,25+,26+,27-,28+/m0/s1

1-[4-[(2S,3R,4S,5S,6R)-4,5-dihydroxy-6-(hydroxymethyl)-3-[(2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxyoxan-2-yl]oxy-2,6-dihydroxyphenyl]-3-(3-hydroxy-4-methoxyphenyl)propan-1-one

Neohesperidin DC NHDC

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 : ~100 mg/mL (~163.24 mM)

配方 1 中的溶解度: ≥ 2.5 mg/mL (4.08 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.5 mg/mL (4.08 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.5 mg/mL (4.08 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。