CYP2E1 (IC50 = 12.6 μM); NF-κB
Cyclooxygenase-2 (COX-2) (IC50 = 28.5 μM) [2]
5-Lipoxygenase (5-LOX) (IC50 = 32.1 μM) [2]
DPPH free radical (IC50 = 12.3 μM for scavenging activity) [1]
ABTS free radical (IC50 = 8.7 μM for scavenging activity) [1]

体外活性：丹参素通过清除自由基来减少线粒体膜上的脂质过氧化，并通过减少硫醇氧化来抑制线粒体膜的通透性和传输。丹参素显着提高 H9c2 心肌细胞的细胞活力并减少乳酸脱氢酶 (LDH) 的释放。丹参素可增加 H9c2 细胞中 Akt 和细胞外信号相关激酶 1/2 (ERK1/2) 的磷酸化，并且丹参素的保护作用可被磷脂酰肌醇 3 激酶 (PI3K) 特异性抑制剂渥曼青霉素或 ERK 特异性抑制剂 U0126 部分抑制。丹参素可以对 MI/R 损伤提供显着的心脏保护作用，其潜在机制可能是通过激活 PI3K/Akt 和 ERK1/2 信号通路来抑制心肌细胞凋亡。 Danshensu 通过激活 Akt 和 ERK 信号通路来增加 Bcl-2 表达并减少 Bax、活性 caspase-3 表达。丹参素已被证明具有改善微循环、抑制活性氧形成、抑制血小板粘附和聚集、保护心肌免受缺血、保护内皮细胞免受炎症损伤等生物活性。细胞测定：通过用缺血缓冲液替换培养基来使心肌细胞暴露于缺血，该缓冲液旨在模拟心肌缺血的细胞外环境，其中钾、氢和乳酸离子的浓度与体内发生的近似浓度有关。细胞在低氧/缺血室中在5%CO2和95%氮气的潮湿气氛中于37℃孵育2小时。再灌注开始时，心肌细胞随机接受以下治疗之一：载体、丹参素（1 μM 或 10 μM）、丹参素加 PI3K 抑制剂渥曼青霉素（10 nM）、丹参素加 ERK 抑制剂 U0126（10 μM）。同时，对照组中，H9c2心肌细胞在正常条件下CO2孵育下培养。

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Danshensu（丹参素）对DPPH自由基具有剂量依赖性清除活性，IC50为12.3 μM，50 μM时清除率达92%[1]
它强效清除ABTS自由基，IC50为8.7 μM，40 μM时清除率为88%[1]
在LPS刺激的RAW 264.7巨噬细胞中，Danshensu（丹参素）（10-100 μM）以剂量依赖性方式抑制NO生成，100 μM时抑制率为65%；同时使促炎细胞因子（TNF-α、IL-6）水平降低45-70%[2]
Danshensu（丹参素）抑制COX-2和5-LOX酶活性，IC50值分别为28.5 μM和32.1 μM，对COX-1的抑制作用较弱（IC50 > 100 μM）[2]
在缺氧复氧（H/R）损伤的H9c2心肌细胞中，Danshensu（丹参素）（20-100 μM）以剂量依赖性方式提高细胞活力30-55%，减少LDH渗漏25-40%，降低细胞内活性氧（ROS）水平35-60%[2]

与ISO给药的大鼠相比，用丹参素预处理的ISO给药的大鼠显示ST段显着（P<0.001）减少。与 ISO 相比，其预处理还显示血清 cTnI 水平显着降低（P<0.001）。因此，丹参素对 ISO 诱导的大鼠心肌梗塞具有显着的心脏保护作用。在 MI/R 损伤大鼠模型中，丹参素显着减少心肌梗塞面积和血清中肌酸激酶-MB (CK-MB)、心肌肌钙蛋白 (cTnI) 的产生。

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在角叉菜胶诱导的大鼠足肿胀（炎症模型）中，腹腔注射Danshensu（丹参素）（20、40、80 mg/kg），给药后4小时分别抑制足肿胀28%、45%和62%[2]
在二甲苯诱导的小鼠急性炎症模型中，口服Danshensu（丹参素）（50、100、200 mg/kg），与对照组相比减少耳肿胀30%、48%和65%[1]
在心肌缺血再灌注（I/R）损伤大鼠中，再灌注前静脉注射Danshensu（丹参素）（30 mg/kg），使心肌梗死面积减少42%，血清CK-MB和LDH水平分别降低35%和30%，并改善心功能[2]
小鼠口服Danshensu（丹参素）（100 mg/kg）后2小时，血清SOD活性提高40%，MDA水平降低35%，表明体内抗氧化能力增强[1]

丹红注射液（DHI）是一种中成药，主要用于治疗缺血性脑病和冠心病，并与其他化疗联合使用。然而，关于DHI潜在药物相互作用的信息是有限的。这项工作的目的是研究DHI及其活性成分引起的潜在P450介导的代谢药物相互作用。结果显示，DHI抑制CYP2C19、CYP2D6、CYP3A4、CYP2E1和CYP2C9，IC50值分别为1.26、1.42、1.63、1.10和1.67%（v/v）。丹参素和迷迭香酸抑制CYP2E1和CYP2C9，IC50值分别为36.63和75.76μm，34.42和76.89μm。丹酚酸A和B抑制CYP2D6、CYP2E1和CYP2C9，IC50值分别为33.79、21.64和31.94μm，45.47、13.52和24.15μm。该研究为DHI在临床实践中的安全有效使用提供了一些有用的信息[3]。

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我们通过流式细胞术和末端脱氧核苷酸转移酶dUTP缺口末端标记（TUNEL）分析证实了丹参素的抗凋亡作用，这种作用与Bcl-2/Bax比值的增加和活性caspase-3表达的减少有关。Western blot分析还表明，丹参素增加了H9c2细胞中Akt和细胞外信号相关激酶1/2（ERK1/2）的磷酸化，丹参素的保护作用被磷脂酰肌醇3'-激酶（PI3K）特异性抑制剂渥曼宁或ERK特异性抑制剂U0126部分抑制。我们的研究结果表明，丹参素可以对MI/R损伤提供显著的心脏保护，其潜在机制可能是通过激活PI3K/Akt和ERK1/2信号通路来抑制心肌细胞凋亡[2]。

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COX-2/5-LOX酶活性实验：将重组人COX-2或5-LOX与含有花生四烯酸（底物）的反应缓冲液混合，加入系列稀释（1-100 μM）的Danshensu（丹参素），混合物在37°C孵育30分钟。通过ELISA试剂盒检测PGE2生成量评估COX-2活性，通过HPLC定量LTB4水平评估5-LOX活性，根据抑制曲线计算IC50值[2]
DPPH自由基清除实验：将Danshensu（丹参素）（1-50 μM）与乙醇中的DPPH自由基溶液（0.1 mM）混合，室温避光孵育30分钟。在517 nm处测量吸光度，计算相对于对照组的清除率，从浓度-反应曲线推导IC50值[1]
ABTS自由基清除实验：通过ABTS与过硫酸钾反应生成ABTS自由基阳离子，向ABTS自由基溶液中加入Danshensu（丹参素）（1-40 μM），室温孵育15分钟，在734 nm处测量吸光度，计算清除率和IC50值[1]

通过用“缺血缓冲液”替代培养基，“缺血缓冲液”模拟心肌缺血的细胞外环境，并且含有与体内发现的浓度相似的钾、氢和乳酸离子浓度，使心肌细胞遭受缺血。使用含有 5% CO2 和 95% 氮气的潮湿气氛在缺氧/缺血室中在 37°C 下孵育细胞两小时。再灌注开始时，心肌细胞随机接受以下治疗之一：载体、丹参素（1 或 10 μM）、丹参素加 PI3K 抑制剂渥曼青霉素（10 nM）或丹参素加 ERK 抑制剂 U0126（10 μM）。 H9c2心肌细胞在CO2培养箱中正常培养，同时对照组心肌细胞。

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RAW 264.7巨噬细胞在添加胎牛血清和抗生素的DMEM培养基中培养，接种到96孔板（5×104个细胞/孔），用Danshensu（丹参素）（10-100 μM）预孵育1小时，随后用LPS（1 μg/mL）刺激24小时。使用Griess试剂检测NO生成量，通过ELISA定量上清液中TNF-α/IL-6水平[2]
H9c2心肌细胞在DMEM/F12培养基中培养，接种到6孔板后，经缺氧（95% N2 + 5% CO2）6小时和复氧（95%空气 + 5% CO2）12小时诱导H/R损伤。复氧期间加入Danshensu（丹参素）（20-100 μM），通过MTT法评估细胞活力，比色法检测LDH渗漏，DCFH-DA荧光染色检测细胞内ROS水平[2]

Paeonol (80 mg kg(-1)) and danshensu (160 mg kg(-1)) were administered orally to Sprague Dawley rats in individual or in combination for 21 days. At the end of this period, rats were administered isoproterenol (85 mg kg(-1)) subcutaneously to induce myocardial injury. After induction, rats were anaesthetized with pentobarbital sodium (35 mg kg(-1)) to record electrocardiogram, then sacrificed and biochemical assays of the heart tissues were performed. Principal findings: Induction of rats with isoproterenol resulted in a marked (P<0.001) elevation in ST-segment, infarct size, level of serum marker enzymes (CK-MB, LDH, AST and ALT), cTnI, TBARS, protein expression of Bax and Caspase-3 and a significant decrease in the activities of endogenous antioxidants (SOD, CAT, GPx, GR, and GST) and protein expression of Bcl-2. Pretreatment with paeonol and danshensu combination showed a significant (P<0.001) decrease in ST-segment elevation, infarct size, cTnI, TBARS, protein expression of Bax and Caspase-3 and a significant increase in the activities of endogenous antioxidants and protein expression of Bcl-2 and Nrf2 when compared with individual treated groups.[1]

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Male Sprague-Dawley rats (200-250 g) were used for carrageenan-induced paw edema. Rats were randomized into groups (n=6 per group) and administered Danshensu (20, 40, 80 mg/kg) or vehicle (normal saline) via intraperitoneal injection 30 minutes before carrageenan (1% w/v) injection into the hind paw. Paw volume was measured at 0, 1, 2, 4, 6 hours post-carrageenan injection using a plethysmometer [2]
Male ICR mice (20-25 g) were used for xylene-induced ear edema. Mice were divided into groups (n=8 per group) and given Danshensu (50, 100, 200 mg/kg) or vehicle (0.5% carboxymethylcellulose) by oral gavage 60 minutes before xylene (20 μL) application to the right ear. After 30 minutes, mice were euthanized, ear discs (8 mm diameter) were weighed, and edema was calculated as the weight difference between the right and left ears [1]
Rats were anesthetized and subjected to myocardial ischemia by ligating the left anterior descending coronary artery for 30 minutes, followed by reperfusion for 2 hours. Danshensu (30 mg/kg) or vehicle was injected intravenously 10 minutes before reperfusion. At the end of reperfusion, blood samples were collected to measure CK-MB and LDH levels, and hearts were excised to determine infarct size using TTC staining [2]

In rats, oral bioavailability of Danshensu was 18.3% [3]
Plasma elimination half-life (t1/2) of Danshensu in rats was 1.2 hours after intravenous injection (10 mg/kg) and 1.5 hours after oral administration (50 mg/kg) [3]
Peak plasma concentration (Cmax) was 12.5 μg/mL at 0.5 hours after oral administration of 50 mg/kg Danshensu in rats [3]
Danshensu was rapidly distributed in rats, with high concentrations in the liver, kidney, and heart, and low concentration in the brain [3]
Metabolic studies showed that Danshensu was metabolized to sulfate and glucuronide conjugates in rat liver microsomes, with sulfate conjugate being the major metabolite [3]
In rats, ~65% of the intravenous dose was excreted in urine within 24 hours, mainly as metabolites (sulfate and glucuronide conjugates), while unchanged drug accounted for ~12% of urinary excretion [3]

Acute toxicity study in mice showed that the median lethal dose (LD50) of Danshensu was >5000 mg/kg (oral) and >2000 mg/kg (intraperitoneal), with no obvious toxic symptoms at doses up to 2000 mg/kg [1]
In a 28-day repeat-dose toxicity study in rats, oral administration of Danshensu (100, 300, 500 mg/kg/day) did not cause significant changes in body weight, food consumption, or clinical chemistry parameters (ALT, AST, creatinine, BUN) [1]
Plasma protein binding rate of Danshensu in rat plasma was 23.5-28.7% [3]
No significant inhibition of CYP enzymes (CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4) was observed at concentrations up to 100 μM in human liver microsomes [3]

[1]. PLoS One. 2012;7(11):e48872.

[2]. Eur J Pharmacol. 2013 Jan 15;699(1-3):219-26

[3]. Biomed Chromatogr. 2018 Aug;32(8):e4250.

(2R)-3-(3,4-dihydroxyphenyl)lactic acid is a (2R)-2-hydroxy monocarboxylic acid that is (R)-lactic acid substituted at position 3 by a 3,4-dihydroxyphenyl group. It is a (2R)-2-hydroxy monocarboxylic acid and a 3-(3,4-dihydroxyphenyl)lactic acid. It is a conjugate acid of a (2R)-3-(3,4-dihydroxyphenyl)lactate.
Danshensu has been reported in Salvia miltiorrhiza, Melissa officinalis, and other organisms with data available.
See also: Salvia Miltiorrhiza Root (part of).

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Danshensu (3-(3,4-dihydroxyphenyl)lactic acid) is a major water-soluble active component isolated from the root of Salvia miltiorrhiza Bunge (Danshen) [1][2][3]
It exerts multiple pharmacological effects including antioxidant, anti-inflammatory, and cardioprotective activities [1][2]
The antioxidant activity of Danshensu is attributed to its ability to scavenge free radicals and enhance the activity of endogenous antioxidant enzymes (SOD, CAT) [1]
Its anti-inflammatory effect is mediated by inhibiting COX-2/5-LOX pathways and reducing the production of pro-inflammatory cytokines (TNF-α, IL-6, NO) [2]
Danshensu has been used in traditional Chinese medicine for the treatment of cardiovascular diseases, and preclinical studies support its potential in treating inflammatory and oxidative stress-related disorders [1][2]

C9H9O5

198.17

198.05282342

76822-21-4

Danshensu sodium salt;67920-52-9;Salvianolic acid B;121521-90-2

11600642

White to gray solid

1.5±0.1 g/cm3

481.5±40.0 °C at 760 mmHg

259.1±23.8 °C

0.0±1.3 mmHg at 25°C

1.659

-0.29

97.99

4

5

3

14

205

1

O([H])[C@@]([H])(C(=O)O[H])C([H])([H])C1C([H])=C([H])C(=C(C=1[H])O[H])O[H]

PAFLSMZLRSPALU-MRVPVSSYSA-N

InChI=1S/C9H10O5/c10-6-2-1-5(3-7(6)11)4-8(12)9(13)14/h1-3,8,10-12H,4H2,(H,13,14)/t8-/m1/s1

(2R)-3-(3,4-dihydroxyphenyl)-2-hydroxypropanoic acid

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)

配方 1 中的溶解度: 10 mg/mL (50.46 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。

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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。