Loureirin A
(Synonyms: 龙血素 A) 目录号 : GC32510
Loureirin A is a flavonoid extracted from the red resin of the herbs of Dracaena cochinchinensis, which is known as Dragon's Blood. Loureirin A inhibits platelet activation by an impairment of PI3K/Akt signaling. Loureirin A inhibits Akt phosphorylation.
Cas No.:119425-89-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Loureirin A is a flavonoid extracted from the red resin of the herbs of Dracaena cochinchinensis, which is known as Dragon's Blood. Loureirin A inhibits platelet activation by an impairment of PI3K/Akt signaling. Loureirin A inhibits Akt phosphorylation.
[1] Hong-Zhen Hao, et al. Eur J Pharmacol. 2015 Jan 5;746:63-9.
| Cas No. | 119425-89-7 | SDF | |
| 别名 | 龙血素 A | ||
| Canonical SMILES | O=C(C1=CC=C(O)C=C1)CCC2=CC=C(OC)C=C2OC | ||
| 分子式 | C17H18O4 | 分子量 | 286.32 |
| 溶解度 | DMSO : ≥ 86.6 mg/mL (302.46 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 | 3.4926 mL | 17.463 mL | 34.926 mL |
| 5 mM | 0.6985 mL | 3.4926 mL | 6.9852 mL |
| 10 mM | 0.3493 mL | 1.7463 mL | 3.4926 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。
Loureirin A Exerts Antikeloid Activity by Antagonizing the TGF- β 1/Smad Signalling Pathway
Evid Based Complement Alternat Med 2022 Jul 15;2022:8661288.PMID:35873644DOI:10.1155/2022/8661288.
It has been recently shown that Loureirin A (LA), a major active component of resina draconis, might be effective in the prevention and treatment of liver fibrosis. We examined whether LA could inhibit the formation of keloids. To investigate the pharmacological effects of Loureirin A on keloid formation and the underlying mechanisms. CellTiter-Blue viability assays were used to examine the proliferation of keloid fibroblasts (KFs) that were treated with LA. Fibroblast migration was evaluated using a cell migration assay. Immunofluorescence staining was used to measure the expression of α-SMA in KFs. RT-qPCR was used to evaluate the mRNA expression of Col-I, Col-III, α-SMA, Bax, and Caspase-3, while Western blotting was used to evaluate the protein expression of Col-I, Col-III, α-SMA, Bax, Caspase-3, p-Smad2, and p-Smad3. LA inhibited the proliferation of KFs and suppressed the migration and TGF-β1-induced myofibroblast differentiation of KFs. In addition, LA downregulated the mRNA and protein levels of Col-I, Col-III, and α-SMA while promoting the mRNA and protein levels of Bax and Caspase-3. Moreover, LA downregulated the protein levels of p-Smad2 and p-Smad3 in cultured TGF-β1-treated KFs ex vivo. These results show that LA has an antikeloid effect on KFs by suppressing the TGF-β1/Smad signalling pathway. Our findings suggest that LA may be a potential candidate drug for the prevention and treatment of keloids.
Effect of Loureirin A against Candida albicans biofilms
Chin J Nat Med 2019 Aug;17(8):616-623.PMID:31472899DOI:10.1016/S1875-5364(19)30064-0.
Loureirin A is a major active component of Draconis sanguis, a traditional Chinese medicine. This work aimed to investigate the activity of Loureirin A against Candida albicans biofilms. 2, 3-Bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide (XTT)reduction assay and scanning electron microscopy were used to investigate the anti-biofilm effect. Minimal inhibitory concentration testing and time-kill curve assay were used to evaluate fungicidal activity. Cell surface hydrophobicity (CSH) assay and hyphal formation experiment were respectively carried out to investigate adhesion and morphological transition, two virulence traits of C. albicans. Real-time RT-PCR was used to investigate gene expression. Galleria mellonella-C. albicans and Caenorhabditis elegans-C. albicans infection models were used to evaluate the in-vivo antifungal effect. Human umbilical vein endothelial cells and C. elegans nematodes were used to evaluate the toxicity ofloureirin A. Our data indicated that Loureirin A had a significant effect on inhibiting C. albicans biofilms, decreasing CSH, and suppressing hyphal formation. Consistently, Loureirin A down-regulated the expression of some adhesion-related genes and hypha/biofilm-related genes. Moreover, Loureirin A prolonged the survival of Galleria mellonella and Caenorhabditis elegans in C. albicans infection models and exhibited low toxicity. Collectively, Loureirin A inhibits fungal biofilms, and this effect may be associated with the suppression of pathogenic traits, adhesion and hyphal formation.
miR-203a-3p promotes loureirin A-induced hair follicle stem cells differentiation by targeting Smad1
Anat Rec (Hoboken) 2021 Mar;304(3):531-540.PMID:32589363DOI:10.1002/ar.24480.
MicroRNAs (miRNAs) participate in the repair of skin trauma. Our previous study indicated that Loureirin A promoted hair follicle stem cells (HFSCs) to repair skin epidermis. However, the mechanism of miRNA-mediated regulation of loureirin A-induced HFSC differentiation remained to be explored. In the present study, HFSCs from rat vibrissa were identified by immunofluorescence in vitro. Microarray and quantitative real time polymerase chain reaction analyses demonstrated that miR-203a-3p was upregulated in differentiated HFSCs induced by Loureirin A. The expression of cytoskeletal keratin (CK) 5 and involucrin was promoted by miR-203a-3p mimics while repressed by a miR-203a-3p inhibitor. Smad1 was identified as a key target of miR-203a-3p using target prediction tools. Luciferase reporter gene test confirmed a special target association between miR-203a-3p and Smad1. Short interfering Smad1 was transfected into HFSCs, and the expression levels of CK5 and involucrin were upregulated. Thus, it can be inferred that miR-203a-3p negatively regulated the expression of Smad1 and promoted the differentiation of loureirin A-induced HFSCs. Bone morphogenetic protein (BMP) signal inhibition and Wnt activation coregulate skin injury repair. BMP/Smad1 signaling is involved in maintaining the characteristics of HFSCs and inhibiting their differentiation. Our results showed that miR-203a-3p reduces Smad1 to release BMP inhibition. Taken together, miR-203a-3p/Smad1 is a potential therapeutic molecular target in skin wound healing, and may play an active role in wound repair and regenerative medicine.
Antiplatelet activity of Loureirin A by attenuating Akt phosphorylation: In vitro studies
Eur J Pharmacol 2015 Jan 5;746:63-9.PMID:25445049DOI:10.1016/j.ejphar.2014.10.059.
Loureirin A is a flavonoid extracted from Dragon׳s Blood that has been used to promote blood circulation and remove stasis in Chinese traditional medicine. However, the mechanisms of these effects are not fully understood. We explored the anti-platelet activity and underlying mechanism of Loureirin A in vitro. Our results indicated that Loureirin A negatively affected agonist-induced platelet aggregation such as collagen, collagen-related peptide (CRP), ADP and thrombin. Loureirin A inhibited collagen-induced platelet ATP secretion and thrombin-stimulated P-selectin expression in a dose-dependent manner. Platelet spreading on immobilized fibrinogen was significantly impaired in the presence of Loureirin A. Immunoblotting analysis indicated that 100μM of Loureirin A almost completely eliminated collagen-induced Akt phosphorylation at Ser473. Interestingly, a submaximal dose (50μM) of Loureirin A had an additive inhibitory effect with the phosphoinositide 3-kinase (PI3K) inhibitor Ly294002 on collage-induced Akt phosphorylation in platelets. Taken together, Loureirin A had an inhibitory effect on platelet activation, perhaps through an impairment of PI3K/Akt signaling.
miR‑339‑5p negatively regulates Loureirin A‑induced hair follicle stem cell differentiation by targeting DLX5
Mol Med Rep 2018 Aug;18(2):1279-1286.PMID:29901112DOI:10.3892/mmr.2018.9110.
Our previous study indicated that Loureirin A induces hair follicle stem cell (HFSC) differentiation through Wnt/β‑catenin signaling pathway activation. However, if and how microRNAs (miRNAs/miRs) modulate Loureirin A‑induced differentiation remains to be elucidated. In the present study, HFSCs were separated from the vibrissae of rats and identified by CD34 and keratin, type 1 cytoskeletal (K)15 expression. Microarray‑based miRNA profiling analysis revealed that miR‑339‑5p was downregulated in Loureirin A‑induced HFSC differentiation. miR‑339‑5p overexpression by transfection with miR‑339‑5p mimics markedly inhibited the expression of K10 and involucrin, which are markers of epidermal differentiation, whereas inhibition of miR‑339‑5p by miR‑339‑5p inhibitor transfection promoted the expression of K10 and involucrin. These results suggest that miR‑339‑5p is a negative regulator of HFSC differentiation following induction by Loureirin A. These findings were confirmed by a luciferase assay. Homeobox protein DLX‑5 (DLX5) was identified as a direct target of miR‑339‑5p. Furthermore, it was demonstrated that miR‑339‑5p inhibited DLX5. Overexpression of miR‑339‑5p by mimic transfection significantly inhibited protein Wnt‑3a (Wnt3a) expression, while inhibition of miR‑339‑5p by inhibitor transfection significantly increased the expression of Wnt3a. Furthermore, small interfering RNA targeting DLX5 was transfected into HFSCs, and western blot analysis revealed that Wnt3a, involucrin and K10 expression was significantly downregulated. Taken together, these results suggest that miR‑339‑5p negatively regulated Loureirin A‑induced HFSC differentiation by targeting DLX5, resulting in Wnt/β‑catenin signaling pathway inhibition. This may provide a possible therapeutic target for skin repair and regeneration.