Dehydrocorydaline chloride
(Synonyms: 盐酸脱氢紫堇碱; 13-Methylpalmatine chloride) 目录号 : GC35832
An alkaloid with diverse biological activities
Cas No.:10605-03-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Dehydrocorydaline is an alkaloid that has been found in C. yanhusuo and has diverse biological activities.1,2,3,4 It is herbicidal against duckweed (L. minor) when used at a concentration of 10 ppm in the growth medium.1 Dehydrocorydaline inhibits serotonin reuptake by organic cation transporter 2 (OCT2) and dopamine reuptake by OCT3 (IC50s = 0.137 and 0.354 ?M, respectively, for human recombinant transporters), as well as reduces dopamine, 5-HT, and norepinephrine reuptake in mouse brain synaptosomes.2 In vivo, dehydrocorydaline (1.5 and 3 mg/kg) decreases immobility time in the forced swim test in a mouse model of depression induced by chronic unpredictable mild stress. Dehydrocorydaline (10 mg/kg) reduces acetic acid-induced writhing in mice and increases the mechanical paw withdrawal threshold in a mouse model of bone cancer pain.3,4
1.Iwasa, K., Moriyasu, M., and Nader, B.Fungicidal and herbicidal activities of berberine related alkaloidsBiosci. Biotechnol. Biochem.64(9)1998-2000(2000) 2.Jin, L., Zhou, S., Zhu, S., et al.Dehydrocorydaline induced antidepressant-like effect in a chronic unpredictable mild stress mouse model via inhibiting uptake-2 monoamine transportersEur. J. Pharmacol.864172725(2019) 3.Yin, Z.-Y., Li, L., Chu, S.-S., et al.Antinociceptive effects of dehydrocorydaline in mouse models of inflammatory pain involve the opioid receptor and inflammatory cytokinesSci. Rep.627129(2016) 4.Huo, W., Zhang, Y., Liu, Y., et al.Dehydrocorydaline attenuates bone cancer pain by shifting microglial M1/M2 polarization toward the M2 phenotypeMol. Pain141744806918781733(2018)
| Cas No. | 10605-03-5 | SDF | |
| 别名 | 盐酸脱氢紫堇碱; 13-Methylpalmatine chloride | ||
| Canonical SMILES | CC1=C(C=CC(OC)=C2OC)C2=C[N+]3=C1C4=CC(OC)=C(OC)C=C4CC3.[Cl-] | ||
| 分子式 | C22H24ClNO4 | 分子量 | 401.88 |
| 溶解度 | DMSO: 25 mg/mL (62.21 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.4883 mL | 12.4415 mL | 24.883 mL |
| 5 mM | 0.4977 mL | 2.4883 mL | 4.9766 mL |
| 10 mM | 0.2488 mL | 1.2442 mL | 2.4883 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
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，
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 saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
PRDX2 removal inhibits the cell cycle and autophagy in colorectal cancer cells
Aging (Albany NY) 2020 Jul 20;12(16):16390-16409.PMID:32692719DOI:10.18632/aging.103690.
Colorectal cancer (CRC) is a prevalent worldwide disease in which the antioxidant enzyme peroxiredoxin 2 (PRDX2) plays an important role. To investigate the molecular mechanism of PRDX2 in CRC, we performed bioinformatics analysis of The Cancer Genome Atlas (TCGA) datasets and Gene Expression Omnibus (GEO) DataSets (accession no. GSE81429). Our results suggest that PRDX2 is associated with cell-cycle progression and autophagy activated by the P38 MAPK/FOXO signaling pathway. Using a short-hairpin RNA vector, we verified that PRDX2 is essential for CRC cell proliferation and S-phase progression. Immunostaining, electron microscopy and western blotting assays verified the effect of PRDX2 knockdown on autophagy flux and p38 activation. The P38 activator Dehydrocorydaline chloride partially rescued the effects of sh-PRDX2 on the expression of proteins related to cell-cycle progression and autophagy. We verified the correlation between PRDX2 expression and the expression of an array of cell-cycle and autophagy-related genes using data from an independent set of 222 CRC patient samples. A mouse xenoplast model was consistent with in vitro results. Our results suggest that PRDX2 promotes CRC cell-cycle progression via activation of the p38 MAPK pathway.
STRIP2 silencing inhibits vascular smooth muscle cell proliferation and migration via P38-AKT-MMP-2 signaling pathway
J Cell Physiol 2019 Dec;234(12):22463-22476.PMID:31093976DOI:10.1002/jcp.28810.
STRIP2 (FAM40B) was reported to regulate tumor cell migration. Our study aims to discuss the effect of STRIP2 in mouse aortic smooth muscle cell (MOVAS) proliferation and migration processes, which contributes greatly to atherosclerosis formation. In MOVAS cells, STRIP2 depletion suppressed cell proliferation and migration, which were related to a remarkable decrease in matrix metalloproteinases-2 (MMP-2)/MMP-9 expression. Additionally, P38 mitogen-activated protein kinases and Protein kinase B (AKT) are inactivated while extracellular signal-regulated kinase (ERK1/2) and jun N-terminal kinase (JNK) are activated upon STRIP2 silencing. SB203580 (P38 inhibitor) further reduced AKT phosphorylation (p-AKT) while Dehydrocorydaline chloride (Dc; P38 activator) reversed this effect. Furthermore, Dc significantly recovered MMP-2 expression in STRIP2-knockdown cells. As expected, overexpressing STRIP2 exhibited a contrary effect. Dc and AKT activator SC79 reversed the inhibition of cell proliferation and migration induced by STRIP2 silencing. Interestingly, STRIP2 depletion increased vascular endothelial growth factor level significantly. Taken together, STRIP2 contributed to cell proliferation and migration through P38-AKT-MMP-2 signaling in MOVAS cells, indicating the importance of STRIP2 in atherosclerosis.