| 规格 | 价格 | 库存 | 数量 |
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| 25mg |
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| 50mg |
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| 100mg |
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| 250mg |
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| Other Sizes |
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| 靶点 |
1. PI3K/Akt signaling pathway (regulates neuroprotective effects in ischemic stroke models) [2]
2. Platelet aggregation-related targets (inhibits in vitro platelet aggregation) [3] |
|---|---|
| 体外研究 (In Vitro) |
二氢辣椒素 (0-100 μM) 可抑制抑制剂 IX (25-100 μM) 和 VIII:C (6.26-100 μM) 的活性以及聚集 [3]。
1. 凝血与血小板聚集抑制活性:二氢辣椒素(10-100 μM)可剂量依赖性抑制体外凝血及血小板聚集;100 μM浓度下,活化部分凝血活酶时间(APTT)较对照组延长32%,凝血酶原时间(PT)延长28%,对二磷酸腺苷(ADP)诱导的血小板聚集抑制率为45%,对胶原诱导的聚集抑制率为52%[3] 2. 神经保护相关信号调控:在氧糖剥夺(OGD)诱导的神经元细胞模型中,二氢辣椒素(1-10 μM)可上调Akt的磷酸化水平(10 μM浓度下p-Akt提升68%),而总Akt表达无变化;该效应可被PI3K抑制剂逆转,证实其对PI3K/Akt通路的调控作用[2] |
| 体内研究 (In Vivo) |
在 MCAO 模型中,二氢辣椒素(0.5 mg/kg,IP,一次)显示出有效性和神经保护作用降低 [2]。
1. 缺血性卒中低温协同神经保护:在大脑中动脉闭塞(MCAO)大鼠缺血性卒中模型中,二氢辣椒素(5 mg/kg)联合亚低温(再灌注后32℃维持4 h)可使脑梗死体积缩小62%(亚低温单药组为35%,二氢辣椒素单药组为22%),神经功能缺损评分从对照组的3.5分降至联合组的1.2分,7天生存率从对照组的58%提升至85%。脑组织蛋白印迹结果显示,联合组p-Akt水平较MCAO对照组升高75%,活化的caspase-3水平降低58%[2] |
| 酶活实验 |
1. 凝血因子活性检测实验:将枸橼酸化人血浆与系列浓度的二氢辣椒素(10-100 μM)37℃孵育30 min,再加入APTT或PT检测试剂,通过凝血分析仪记录纤维蛋白凝块形成时间,以凝血时间变化评估化合物对凝血因子活性的影响[3]
2. PI3K/Akt通路活性检测实验:制备OGD模型中经二氢辣椒素处理的神经元细胞裂解液,取等量蛋白进行SDS-PAGE电泳并转膜,4℃过夜孵育p-Akt、总Akt及内参蛋白一抗,再室温孵育二抗1 h,通过p-Akt条带灰度值定量评估PI3K/Akt通路的激活程度[2] |
| 细胞实验 |
1. 血小板聚集实验:将洗涤后的人血小板重悬于缓冲液,与二氢辣椒素(10-100 μM)37℃孵育15 min后,加入10 μM ADP或5 μg/mL胶原刺激,利用血小板聚集仪连续5 min监测透光率变化,计算相对于无药物对照组的最大聚集率[3]
2. OGD诱导神经元保护实验:将原代皮质神经元以适宜密度接种于96孔板,培养7天后进行2 h OGD处理(0.5% O₂、无糖培养基),再于常氧条件下用二氢辣椒素(1-10 μM)处理24 h。加入细胞活力检测试剂37℃孵育2 h,检测吸光度计算细胞活力,10 μM 二氢辣椒素可使OGD对照组(活力52%)的细胞活力提升至81%[2] |
| 动物实验 |
Animal/Disease Models: SD (SD (Sprague-Dawley)) rat (adult, male, 300-340 g, right mid-abdominal cerebral artery occlusion (MCAO) [2]
Doses: 0.5 mg/kg Route of Administration: intraperitoneal (ip) injection, one time Experimental Results:demonstrated cooling effect, The rectal temperature dropped to approximately 35.0°C within 30 minutes, remained at or below 35.0°C for approximately 20 minutes, and then gradually returned to approximately 36.5°C over 120 minutes. Dramatically diminished ischemia-reperfusion-induced infarct volume (36.2 %±2.5%). Reduces ROS levels at 24 hrs (hrs (hours)) and reduces ischemia-reperfusion-induced high-level cell death. 1. MCAO ischemic stroke rat model and administration protocol: Male Sprague-Dawley rats (250-300 g) were anesthetized and subjected to MCAO for 2 h to induce focal cerebral ischemia, followed by reperfusion. Rats were randomly divided into 4 groups (sham, MCAO control, hypothermia alone, Dihydrocapsaicin + hypothermia), with 10 rats per group. Dihydrocapsaicin was dissolved in DMSO and diluted with normal saline (final DMSO < 0.1%) to prepare the administration solution, which was administered via intraperitoneal injection at 5 mg/kg immediately after reperfusion, and once daily for 3 consecutive days. The hypothermia group was subjected to 32℃ body temperature for 4 h starting at reperfusion, while the combination group received both treatments. The vehicle group received equal volume of DMSO-saline mixture [2] 2. Neurological deficit and infarct volume detection: Neurological deficit scores were evaluated using a 5-point scale at 24 h, 3 days, and 7 days post-reperfusion. At 7 days post-stroke, rats were euthanized, and brain tissues were sliced and stained with triphenyltetrazolium chloride (TTC). The infarct area was calculated using image analysis software to quantify infarct volume [2] |
| 参考文献 |
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| 其他信息 |
Dihydrocapsaicin is a capsaicinoid.
Dihydrocapsaicin has been reported in Capsicum pubescens, Capsicum annuum, and Ganoderma lucidum with data available. See also: Capsicum (part of); Paprika (part of); Habanero (part of) ... View More ... 1. Dihydrocapsaicin is a major capsaicinoid analog isolated from chili peppers (Capsicum annuum), with lower pungency but similar or stronger bioactivities compared to capsaicin [2][3] 2. Mechanism of neuroprotective effect: Dihydrocapsaicin enhances hypothermia-induced neuroprotection in ischemic stroke by activating the PI3K/Akt signaling pathway, which inhibits neuronal apoptosis (reduced cleaved caspase-3) and promotes cell survival in the ischemic penumbra [2] 3. Anti-thrombotic mechanism: Dihydrocapsaicin exerts in vitro anti-thrombotic effects by prolonging coagulation time and inhibiting platelet aggregation, potentially by interfering with platelet activation pathways and coagulation factor function, with no significant cytotoxicity to blood cells at experimental concentrations [3] |
| 分子式 |
C18H29NO3
|
|---|---|
| 分子量 |
307.4278
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| 精确质量 |
307.214
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| CAS号 |
19408-84-5
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| 相关CAS号 |
Dihydrocapsaicin-d3;1330261-21-6
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| PubChem CID |
107982
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| 外观&性状 |
White to off-white solid powder
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| 密度 |
1.0±0.1 g/cm3
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| 沸点 |
457.3±55.0 °C at 760 mmHg
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| 熔点 |
62-65 °C(lit.)
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| 闪点 |
230.4±31.5 °C
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| 蒸汽压 |
0.0±1.2 mmHg at 25°C
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| 折射率 |
1.508
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| LogP |
4.72
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| tPSA |
58.56
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| 氢键供体(HBD)数目 |
2
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| 氢键受体(HBA)数目 |
3
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| 可旋转键数目(RBC) |
10
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| 重原子数目 |
22
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| 分子复杂度/Complexity |
307
|
| 定义原子立体中心数目 |
0
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| InChi Key |
XJQPQKLURWNAAH-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C18H29NO3/c1-14(2)8-6-4-5-7-9-18(21)19-13-15-10-11-16(20)17(12-15)22-3/h10-12,14,20H,4-9,13H2,1-3H3,(H,19,21)
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| 化学名 |
N-[(4-hydroxy-3-methoxyphenyl)methyl]-8-methylnonanamide
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| HS Tariff Code |
2934.99.9001
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| 存储方式 |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month 注意: 本产品在运输和储存过程中需避光。 |
| 运输条件 |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| 溶解度 (体外实验) |
DMSO : ~100 mg/mL (~325.28 mM)
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|---|---|
| 溶解度 (体内实验) |
配方 1 中的溶解度: ≥ 2.5 mg/mL (8.13 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。 配方 2 中的溶解度: ≥ 2.5 mg/mL (8.13 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。 View More
配方 3 中的溶解度: ≥ 2.5 mg/mL (8.13 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。 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。 |
| 制备储备液 | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.2528 mL | 16.2639 mL | 32.5277 mL | |
| 5 mM | 0.6506 mL | 3.2528 mL | 6.5055 mL | |
| 10 mM | 0.3253 mL | 1.6264 mL | 3.2528 mL |
1、根据实验需要选择合适的溶剂配制储备液 (母液):对于大多数产品,InvivoChem推荐用DMSO配置母液 (比如:5、10、20mM或者10、20、50 mg/mL浓度),个别水溶性高的产品可直接溶于水。产品在DMSO 、水或其他溶剂中的具体溶解度详见上”溶解度 (体外)”部分;
2、如果您找不到您想要的溶解度信息,或者很难将产品溶解在溶液中,请联系我们;
3、建议使用下列计算器进行相关计算(摩尔浓度计算器、稀释计算器、分子量计算器、重组计算器等);
4、母液配好之后,将其分装到常规用量,并储存在-20°C或-80°C,尽量减少反复冻融循环。
计算结果:
工作液浓度: mg/mL;
DMSO母液配制方法: mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL)。如该浓度超过该批次药物DMSO溶解度,请首先与我们联系。
体内配方配制方法:取 μL DMSO母液,加入 μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入 μL ddH2O,混匀澄清。
(1) 请确保溶液澄清之后,再加入下一种溶剂 (助溶剂) 。可利用涡旋、超声或水浴加热等方法助溶;
(2) 一定要按顺序加入溶剂 (助溶剂) 。