Plasmodium; anti-malarial

青蒿素 (3.125-100 μM) 浓度依赖性地抑制 Aβ25-35 诱导的 PC12 细胞细胞毒性。青蒿素 (25 μM) 抑制 Aβ25-35 诱导的 LDH 释放、细胞凋亡和 ROS 产生，减弱 Aβ 诱导的线粒体膜电位损失和 caspase 3/7 活性增加，并在一定时间和浓度下刺激 ERK1/2 磷酸化PC12细胞中的依赖性方式。 ERK 1/2通路介导青蒿素对PC12细胞的保护作用[1]。青蒿素在 MCF-7/Dox 细胞系中显示出细胞毒活性，处理 24 小时后 IC50 为 3.7±0.4 μg/mL。此外，青蒿素处理对Dox和DDP敏感和耐药的MCF-7细胞会导致LF、FTH1和HEP等蛋白表达下降。无论由于抑制 VEGF 表达和细胞迁移而导致的氧化应激，青蒿素都会激活 p38 MAPK 激酶级联反应 [2]。 Artemisinin (50、100 或 200 mg) 显着抑制异氟醚诱导的海马神经元损失，减少 caspase-3 阳性细胞计数，同时裂解 caspase-3 表达，并调节凋亡途径蛋白的表达。青蒿素调节 JNK/ERK 1/2 信号传导和组蛋白乙酰化 [3]。青蒿素以剂量依赖性方式抑制 HCV 复制，EC50 值为 167±38 µM。青蒿素及其最有效的类似物通过诱导活性氧 (ROS) 部分抑制 HCV 的体外复制[4]。青蒿素以剂量依赖性方式显着抑制 VSMC 增殖。青蒿素 (1 mM) 72 小时显着降低增殖细胞核抗原信使 RNA 的表达[5]。

青蒿素（50、100 或 200 mg/kg b.wt/天，口服）可预防 T 迷宫测试中观察到的异氟烷引起的工作记忆损伤。青蒿素可增强暴露于异氟醚的大鼠的空间导航和记忆力。与单独暴露于异氟烷的大鼠相比，青蒿素治疗的大鼠表现出明显更好的表现[3]。

活性氧物种测量[2]
分别使用2′，7′-二氯荧光素二乙酸酯（H2DCFDA）和MitoTracker Red CMXRos通过荧光测定法评估细胞内和线粒体ROS的产生。青蒿素处理12小时后，谷氨酸处理12小时，细胞在37°C下在10μmol/L H2DCFDA或0.25μmol/L MitoTracker Red CMXRos中孵育30分钟。然后通过荧光显微镜观察荧光。用530/485nm和579/599nm的激发/发射波长检测荧光。[2]

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线粒体膜电位（ΔΨm）测量[2]
使用四甲基罗丹明乙酯（TMRE）线粒体膜电位测定试剂盒（Abcam，美国）检测线粒体膜电位。细胞在37°C下用20 nM TMRE工作溶液加载20分钟。在蔡司荧光显微镜上观察并获得荧光图像。使用具有594/575nm激发/发射的Tecan Infinite F200板读数器测量荧光强度。

为此，细胞在 96 孔板的 DMEM 中培养，并补充胰岛素。将青蒿素、Dox 和 DDP 以不同浓度添加到培养基中，并将细胞培养 24 或 48 小时。为此目的，青蒿素在培养基中用 0.01% DMSO 稀释。此后，将 10 µL MTT 染料溶液（磷酸盐缓冲盐水中 5 mg/mL）添加到细胞中；将细胞在相同条件下孵育3小时。离心（1500 rpm，5 分钟）后，除去上清液。每孔中加入 100 μL 二甲基亚砜，以溶解甲臜。使用多孔分光光度计在 540 nm 波长下测量吸光度。

[1]. Artemisinin protects PC12 cells against β-amyloid-induced apoptosis through activation of the ERK1/2 signaling pathway. Redox Biol. 2017 Apr 4;12:625-633.

[2]. Artemisinin Prevents Glutamate-Induced Neuronal Cell Death Via Akt Pathway Activation. Front Cell Neurosci. 2018 Apr 20;12:108.

(+)-artemisinin is a sesquiterpene lactone obtained from sweet wormwood, Artemisia annua, which is used as an antimalarial for the treatment of multi-drug resistant strains of falciparum malaria. It has a role as an antimalarial and a plant metabolite. It is a sesquiterpene lactone and an organic peroxide.
Artemisinin has been used in trials studying the treatment of Schizophrenia, Malaria, Falciparum, and Plasmodium Falciparum.
Artemisinin has been reported in Artemisia lancea, Artemisia annua, and other organisms with data available.

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Accumulating evidence displays that an abnormal deposition of amyloid beta-peptide (Aβ) is the primary cause of the pathogenesis of Alzheimer's disease (AD). And therefore the elimination of Aβ is regarded as an important strategy for AD treatment. The discovery of drug candidates using culture neuronal cells against Aβ peptide toxicity is believed to be an effective approach to develop drug for the treatment of AD patients. We have previously showed that artemisinin, a FDA-approved anti-malaria drug, has neuroprotective effects recently. In the present study, we aimed to investigate the effects and potential mechanism of artemisinin in protecting neuronal PC12 cells from toxicity of β amyloid peptide. Our studies revealed that artemisinin, in clinical relevant concentration, protected and rescued PC12 cells from Aβ25-35-induced cell death. Further study showed that artemisinin significantly ameliorated cell death due to Aβ25-35 insult by restoring abnormal changes in nuclear morphology, lactate dehydrogenase, intracellular ROS, mitochondrial membrane potential and activity of apoptotic caspase. Western blotting analysis demonstrated that artemisinin activated extracellular regulated kinase ERK1/2 but not Akt survival signaling. Consistent with the role of ERK1/2, preincubation of cells with ERK1/2 pathway inhibitor PD98059 blocked the effect of artemisinin while PI3K inhibitor LY294002 has no effect. Moreover, Aβ1-42 also caused cells death of PC12 cells while artemisinin suppressed Aβ1-42 cytotoxicity in PC12 cells. Taken together, these results, at the first time, suggest that artemisinin is a potential protectant against β amyloid insult through activation of the ERK1/2 pathway. Our finding provides a potential application of artemisinin in prevention and treatment of AD.[1]

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Artemisinin is an anti-malarial drug that has been in use for almost half century. Recently, novel biological effects of artemisinin on cancer, inflammation-related disorders and cardiovascular disease were reported. However, neuroprotective actions of artemisinin against glutamate-induced oxidative stress have not been investigated. In the current study, we determined the effect of artemisinin against oxidative insult in HT-22 mouse hippocampal cell line. We found that pretreatment of artemisinin declined reactive oxygen species (ROS) production, attenuated the collapse of mitochondrial membrane potential induced by glutamate and rescued HT-22 cells from glutamate-induced cell death. Furthermore, our study demonstrated that artemisinin activated Akt/Bcl-2 signaling and that neuroprotective effect of artemisinin was blocked by Akt-specific inhibitor, MK2206. Taken together, our study indicated that artemisinin prevented neuronal HT-22 cell from glutamate-induced oxidative injury by activation of Akt signaling pathway.[2]

C15H22O5

282.3322

282.146

C, 63.81; H, 7.85; O, 28.33

63968-64-9

Artemisinin-d3;176652-07-6

White to off-white solid powder

1.2±0.1 g/cm3

389.9±42.0 °C at 760 mmHg

156-157ºC

172.0±27.9 °C

0.0±0.9 mmHg at 25°C

1.533

2.27

53.99

O1[C@@]23[C@]4([H])OC([C@]([H])(C([H])([H])[H])[C@]2([H])C([H])([H])C([H])([H])[C@@]([H])(C([H])([H])[H])[C@]3([H])C([H])([H])C([H])([H])C(C([H])([H])[H])(O1)O4)=O

BLUAFEHZUWYNDE-NNWCWBAJSA-N

InChI=1S/C15H22O5/c1-8-4-5-11-9(2)12(16)17-13-15(11)10(8)6-7-14(3,18-13)19-20-15/h8-11,13H,4-7H2,1-3H3/t8-,9-,10+,11+,13-,14-,15-/m1/s1

(3R,5aS,6R,8aS,9R,12S,12aR)-3,6,9-trimethyloctahydro-12H-3,12-epoxy[1,2]dioxepino[4,3-i]isochromen-10(3H)-one

qinghaosu; NSC-369397; NSC369397; Arteannuin; Huanghuahaosu; Artemisinine; Artemisine; (+)-Artemisinin; NSC 369397

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 : 50~56 mg/mL (177.10~198.34 mM)
H2O : < 0.1 mg/mL

配方 1 中的溶解度: ≥ 2.08 mg/mL (7.37 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 (7.37 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 (7.37 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 储备液添加到 900 μL 玉米油中并混合均匀。

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配方 4 中的溶解度: 3% DMSO+ 97% Corn oil: 6mg/ml (21.25mM)

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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。