Treatment with benserazide hydrochloride (BH) and levodopa (LD) alone or in combination (benserazide hydrochloride + LD) (25 μM; 0 hours, 12 hours, 24 hours, and 168 hours; SH-SY5Y) decreases protein aggregation and can limit protein aggregation. Amyloid-induced cytotoxicity in human neuroblastoma cell lines. Both benserazide hydrochloride and LD can be efficient inhibitors of the formation of cytotoxic HSA aggregates, and the inhibitory effect is more visible when the two medicines are introduced at the same time [2].

单独使用盐酸苄丝肼 (BH) 和左旋多巴 (LD) 或联合使用（盐酸苄丝肼 + LD）（25 μM；0 小时、12 小时、24 小时和 168 小时；SH-SY5Y）可减少蛋白质聚集并限制蛋白质聚合。淀粉样蛋白诱导的人神经母细胞瘤细胞系的细胞毒性。盐酸苄丝肼和LD均可有效抑制细胞毒性HSA聚集体的形成，且两种药物同时使用时抑制效果更加明显[2]。

苄丝肼（5-50 mg/kg；腹腔注射；雄性 Wistar 大鼠）治疗可提高外源性 L-DOPA 衍生的细胞外 DA 水平，并显着延长 6-OHDA 损伤大鼠达到峰值 DA 水平的时间。 ..取决于。使用 10 mg/kg 和 50 mg/kg 苄丝肼，去神经纹状体组织中的 AADC 活性显着降低。苄丝肼通过降低黑质纹状体去神经大鼠纹状体中枢 AADC 活性来改变外源性 L-DOPA 的代谢 [1]。

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在假损伤（完整）大鼠中，腹腔注射 50 mg/kg Benserazide hydrochloride 显著降低了纹状体内源性细胞外多巴胺水平，在注射后100分钟达到最低点，为基线水平的53%。较低剂量（5和10 mg/kg）则诱导了短暂但不显著的下降，随后略有上升。[1]
在6-羟基多巴胺（6-OHDA）损伤大鼠（多巴胺能去神经支配模型）的纹状体中，与外源性L-DOPA（50 mg/kg, i.p.）联用前30分钟，使用 Benserazide hydrochloride（5, 10, 或 50 mg/kg, i.p.）进行预处理，与溶剂预处理相比，在320分钟内显著增加了由外源性L-DOPA衍生的细胞外多巴胺累积量。[1]
在L-DOPA给药后，10 mg/kg Benserazide hydrochloride 预处理组的细胞外多巴胺峰值最高。然而，与溶剂组（80分钟）或较低剂量组（5和10 mg/kg组为100分钟）相比，50 mg/kg剂量组达到峰值多巴胺水平的时间显著延长（140分钟）。[1]
腹腔注射 Benserazide hydrochloride（10 和 50 mg/kg）在给药60分钟后，显著抑制了在假损伤和6-OHDA损伤大鼠纹状体组织匀浆中测得的中央AADC活性。[1]
在假损伤大鼠中，10 mg/kg Benserazide hydrochloride 使AADC活性降至溶剂对照组的72%，50 mg/kg 则降至22%。[1]
在6-OHDA损伤大鼠中，10 mg/kg Benserazide hydrochloride 使AADC活性降至溶剂对照组的25%，50 mg/kg 则降至12%。去神经支配纹状体中剩余的AADC活性（溶剂组）约为假损伤大鼠的41%。[1]

离体AADC活性测定： 给大鼠腹腔注射 Benserazide hydrochloride（10 或 50 mg/kg）或溶剂。60分钟后，处死动物并迅速取脑。在冰上分离纹状体，用蔗糖溶液匀浆并离心。将上清液在37°C下孵育20分钟，反应混合物含有磷酸钠缓冲液（pH 7.2）、磷酸吡哆醛、帕吉林、2-巯基乙醇、EDTA、抗坏血酸以及作为底物的L-DOPA。反应用含有内标的高氯酸终止。离心和过滤后，使用高效液相色谱-电化学检测法（HPLC-ECD）定量上清液中形成的多巴胺量。AADC活性表示为每毫克纹状体组织在20分钟孵育内形成的多巴胺纳摩尔数。[1]

细胞活力测定[2]
细胞类型： SH-SY5Y 细胞
测试浓度： 25 μM
孵育时间： > 0 小时、12 小时、24 小时和 168 小时
实验结果：增强细胞活力并抑制细胞毒性人血清白蛋白 (HSA) 聚集体的形成。

Animal/Disease Models: Male Wistar rat 6-hydroxydopamine (6-OHDA) (8 Ag/4 Al)[1]
Doses: 5 mg/kg, 10 mg/kg or 50 mg/kg (pharmacokinetic/PK/PK study) Give Medication: intraperitoneal (ip) injection.
Experimental Results: Extracellular DA levels derived from exogenous L-DOPA increased, and the time to reach peak DA levels was Dramatically prolonged in a dose-dependent manner. AADC activity in denervated striatal tissue was Dramatically diminished at 10 mg/kg and 50 mg/kg.

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Animal Model Preparation: Male Wistar rats (220-250 g) were used. For the dopaminergic denervation model, rats were anesthetized and a stereotaxic injection of 6-hydroxydopamine (6-OHDA, 8 µg in 4 µl) was made into the right medial forebrain bundle. Rats were pretreated with desipramine (25 mg/kg, i.p.) 30 minutes before 6-OHDA injection to protect noradrenergic neurons. Sham-lesioned rats received a saline injection. Two weeks post-surgery, successful denervation was confirmed by apomorphine-induced rotation ( >20 contralateral turns/5 min). Microdialysis experiments were performed 3-4 weeks after surgery.[1]
In Vivo Microdialysis: A guide cannula was implanted into the right striatum. A microdialysis probe was inserted and perfused with artificial Ringer’s solution at 2 µl/min. Dialysates were collected every 20 minutes. After stable baseline DA levels were established (~3 hours), Benserazide hydrochloride (5, 10, or 50 mg/kg, dissolved in saline) or vehicle was administered intraperitoneally (i.p.). In 6-OHDA-lesioned rat experiments, Benserazide hydrochloride or vehicle was administered i.p., followed 30 minutes later by L-DOPA methyl ester hydrochloride (50 mg/kg, i.p., dissolved in saline). Extracellular DA levels in dialysates were measured by HPLC-ECD.[1]
Ex Vivo Tissue Analysis for AADC Activity: Separate groups of rats (sham-lesioned and 6-OHDA-lesioned) were administered Benserazide hydrochloride (10 or 50 mg/kg, i.p.) or vehicle. Sixty minutes later, rats were decapitated, striatal tissues were rapidly dissected, and AADC activity was measured as described in the "Enzyme Assay" section.[1]

This study does not provide data on the absorption, distribution, metabolism, excretion, half-life, or oral bioavailability of Benserazide hydrochloride. It does cite an estimation from another study that the brain tissue concentration of benserazide after a 50 mg/kg injection is approximately 1 µM.[1]

This study does not provide specific toxicity data for Benserazide hydrochloride, such as LD50, organ toxicity, drug-drug interactions, or plasma protein binding. The observed decrease in endogenous striatal DA at a high dose (50 mg/kg) in intact rats is a pharmacological effect related to its mechanism of action.[1]

[1]. Effects of benserazide on L-DOPA-derived extracellular dopamine levels and aromatic L-amino acid decarboxylase activity in the striatum of 6-hydroxydopamine-lesioned rats. Tohoku J Exp Med. 2003 Mar;199(3):149-59.

[2]. A multiparametric analysis of the synergistic impact of anti-Parkinson's drugs on the fibrillation of human serum albumin. Biochim Biophys Acta Proteins Proteom. 2019 Mar;1867(3):275-285.

Benserazide hydrochloride is a hydrochloride that is the monohydrochloride salt of benserazide. An aromatic-L-amino-acid decarboxylase inhibitor (DOPA decarboxylase inhibitor) that does not enter the central nervous system, it is used as an adjunct to levodopa in the treatment of parkinsonism. By preventing the conversion of levodopa to dopamine in the periphery, it causes an increase in the amount of levodopa reaching the central nervous system and so reduces the required dose. Benserazide hydrochloride has no antiparkinson actions when given alone. It has a role as an antiparkinson drug, an EC 4.1.1.28 (aromatic-L-amino-acid decarboxylase) inhibitor and a dopaminergic agent. It contains a benserazide(1+).

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Benserazide hydrochloride is a peripheral aromatic L-amino acid decarboxylase (AADC) inhibitor commonly used in combination with L-DOPA for the treatment of Parkinson's disease to prevent the peripheral conversion of L-DOPA to dopamine, thereby increasing L-DOPA availability to the brain and reducing peripheral side effects.[1]
This study demonstrates that Benserazide hydrochloride also has a central effect by inhibiting AADC activity within the brain (striatum) of both intact rats and rats with dopaminergic denervation (6-OHDA-lesioned model).[1]
The central inhibition of AADC by Benserazide hydrochloride influences the metabolism of exogenous L-DOPA in the denervated striatum. While peripheral inhibition increases L-DOPA bioavailability and thus striatal DA levels, central inhibition can attenuate the conversion of L-DOPA to DA within the brain, leading to a more sustained DA release profile (prolonged time to peak) at higher doses (e.g., 50 mg/kg).[1]
The study suggests that the optimal ratio of L-DOPA to benserazide to maximize striatal extracellular DA is around 5:1 (50 mg/kg L-DOPA : 10 mg/kg benserazide in rats), which aligns with clinical observations.[1]
The findings indicate that the central activity of AADC inhibitors like Benserazide hydrochloride should be considered in both experimental designs and clinical applications for Parkinson's disease, as it can modulate the pharmacokinetics and effects of L-DOPA therapy.[1]

C10H16CLN3O5

293.7041

293.077

14919-77-8

Benserazide;322-35-0;Benserazide-d3 hydrochloride

26964

White to off-white solid powder

574.2ºC at 760 mmHg

146°C

0.527

148.07

8

7

5

19

278

0

ULFCBIUXQQYDEI-UHFFFAOYSA-N

InChI=1S/C10H15N3O5.ClH/c11-6(4-14)10(18)13-12-3-5-1-2-7(15)9(17)8(5)16;/h1-2,6,12,14-17H,3-4,11H2,(H,13,18);1H

2-amino-3-hydroxy-N'-[(2,3,4-trihydroxyphenyl)methyl]propanehydrazide;hydrochloride

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将本产品存放在密封且受保护的环境中，避免吸湿/受潮。

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 (~340.48 mM)
H2O : ≥ 50 mg/mL (~170.24 mM)

配方 1 中的溶解度: ≥ 2.08 mg/mL (7.08 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 20.8 mg/mL澄清DMSO储备液加入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: ≥ 2.08 mg/mL (7.08 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 20.8 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: ≥ 2.08 mg/mL (7.08 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 20.8 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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配方 4 中的溶解度: 100 mg/mL (340.48 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶.

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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。