Magnoflorine
(Synonyms: 木蘭花鹼,Magnoflorine; α-Magnoflorine; Thalictrine) 目录号 : GC41370
An alkaloid
Cas No.:2141-09-5
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Magnoflorine is an alkaloid and a major constituent of S. acutum that has diverse biological activities. It reduces hemolysis induced by lysophosphatidylcholine (LPC), but not NaCl, in a rat erythrocyte suspension when used at concentrations ranging from 0.01 to 10 μM. Magnoflorine (10 μM) induces intracellular chloride influx in neuroblastoma cells, an effect that is reversed by the GABAA receptor antagonist bicuculline . It reduces TNF-α-induced NF-κB expression as well as production of IL-6 and IL-8 in BEAS-2B cells. In vivo, magnoflorine (20 mg/kg, i.p.) improves short- and long-term memory acquisition in a passive avoidance test in a mouse model of scopolamine-induced memory impairment.
| Cas No. | 2141-09-5 | SDF | |
| 别名 | 木蘭花鹼,Magnoflorine; α-Magnoflorine; Thalictrine | ||
| Canonical SMILES | OC1=C(OC)C=C2CC[N+](C)(C)[C@@]3([H])CC4=CC=C(OC)C(O)=C4C1=C32 | ||
| 分子式 | C20H24NO4 | 分子量 | 342.4 |
| 溶解度 | DMF: 100 mg/ml,DMSO: 100 mg/ml,Ethanol: 50 mg/ml,PBS (pH 7.2): 10 mg/ml | 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.9206 mL | 14.6028 mL | 29.2056 mL |
| 5 mM | 0.5841 mL | 2.9206 mL | 5.8411 mL |
| 10 mM | 0.2921 mL | 1.4603 mL | 2.9206 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。
Magnoflorine: A review of its pharmacology, pharmacokinetics and toxicity
Pharmacol Res 2020 Feb;152:104632.PMID:31911246DOI:10.1016/j.phrs.2020.104632.
Magnoflorine is an important quaternary aporphine alkaloid that is isolated from some commonly used herbal medicines (e.g., Sinomenium acutum (Thunb.) Rehder & E.H.Wilson and Coptis chinensis Franch.). In recent years, Magnoflorine has received increasing attention due to its multiple pharmacological activities. This review provides the first comprehensive summary of the plant sources, pharmacological effects, toxicity, and pharmacokinetic characteristics of Magnoflorine. The results indicated that Magnoflorine possesses a wide spectrum of pharmacological properties, including anti-diabetic, anti-inflammatory, neuropsychopharmacological, immunomodulatory, hypotensive, antioxidant, and antifungal activities. Pharmacokinetic studies have shown that Magnoflorine has low bioavailability and high absorption and elimination rates. However, the other compounds (e.g., berberine) present in herbal medicines could reduce the absorption and removal rates of Magnoflorine and increase its bioavailability. Moreover, toxicity studies have suggested that Magnoflorine is non-toxic to most cells. However, long-term and high-dose toxicity testing in animals is still lacking. In view of good pharmacological activities, Magnoflorine is expected to be a potential drug candidate for the treatment of diabetes, depression, or Alzheimer's disease. However, further studies are needed to elucidate its molecular mechanisms and targets, clarify its toxicity, and improve its oral bioavailability.
Magnoflorine prevent the skeletal muscle atrophy via Akt/mTOR/FoxO signal pathway and increase slow-MyHC production in streptozotocin-induced diabetic rats
J Ethnopharmacol 2021 Mar 1;267:113510.PMID:33141056DOI:10.1016/j.jep.2020.113510.
Ethnopharmacological relevance: Tinospora cordifolia (TC) is being used as a blood purifier in Ayurveda since ancient time. It is a very popular immunomodulator and holds anti-inflammatory and anti-oxidative potential, hence anti-aging properties. Therefore, it is also known as 'Amrita' in Ayurveda and is widely used to treat diabetes mellitus type II (T2DM) and its secondary complications; however, its underlying mechanism was not expedited to date. AIM-: To explore the in vivo therapeutic efficiency and mechanism of action of TC and its secondary constitute Magnoflorine on the skeletal muscle atrophy in the rat model of T2DM. Method: Animal model of T2DM was developed using streptozotocin (STZ) injection followed by intervention with TC, metformin, and Magnoflorine for three weeks. Confirmation of T2DM and abrogation of atrophic markers and possible mechanisms on supplementation of TC and Magnoflorine were explored using histology, bio-assays, Western blotting, and q-PCR. Result: TC and Magnoflorine supplementations significantly (p ≤ 0.05) decreased the fasting blood glucose (FBG) levels in T2DM rats. Both treatments prevented the lean body, individual skeletal muscle mass, and myotubes diameter loss (p ≤ 0.05). Magnoflorine significantly reduced the degradation of the protein indicated by biochemical markers of atrophy i.e. decreased serum creatine kinase (CK) levels and increased myosin heavy chain-β (MyHC-β) levels in muscles. Q-PCR and western blotting supported the findings that Magnoflorine significantly increased the mRNA and protein abundances (~3 fold) of MyHC-β.TC and Magnoflorine efficiently decreased the expression of ubiquitin-proteasomal E3-ligases (Fn-14/TWEAK, MuRF1, and Atrogin 1), autophagy (Bcl-2/LC3B), and caspase related genes along with calpains activities in T2DM rats. Both TC and Magnoflorine also increased the activity of superoxide dismutase, GSH-Px, decreased the activities of β-glucuronidase, LPO, and prevented any alteration in the catalase activity. In contrast, Magnoflorine increased expression of TNF-α and IL-6 whereas TC and metformin efficiently decreased the levels of these pro-inflammatory cytokines (p ≤ 0.05). However, Magnoflorine was found to increase phosphorylation of Akt more efficiently than TC and metformin. Conclusion: TC, and Magnoflorine are found to be effective to control fasting blood glucose levels significantly in T2DM rats. It also promoted the Akt phosphorylation, suppressed autophagy and proteolysis that might be related to blood glucose-lowering efficacy of Magnoflorine and TC. However, increased muscle weight, specifically of the soleus muscle, expression of IL-6, and slow MyHC indicated the increased myogenesis in response to Magnoflorine and independent from its hypoglycemic activity.
Magnoflorine improves sensitivity to doxorubicin (DOX) of breast cancer cells via inducing apoptosis and autophagy through AKT/mTOR and p38 signaling pathways
Biomed Pharmacother 2020 Jan;121:109139.PMID:31707337DOI:10.1016/j.biopha.2019.109139.
Breast cancer is a leading cause of cancer death among women worldwide. Doxorubicin (DOX) is a broad-spectrum anti-breast cancer agent, but its clinical use is restricted due to irreversible tissue toxicity. Thereby, new therapeutic approaches are urgently required to promote the sensitivity of breast cancer cells to DOX. Magnoflorine (Mag), a quaternary alkaloid isolated from Chinese herb Magnolia or Aristolochia, has various biological activities, such as anti-inflammation, anti-cancer, and anti-anxiety. In the study, we explored the effects Mag on the sensitivity of breast cancer cells to DOX. We demonstrated that Mag strongly promoted DOX-induced anti-proliferative effects in breast cancer cells while not in normal cells. Mag addition markedly promoted the effects of DOX on the inhibition of migration and invasion in breast cancer cells. DOX-triggered DNA damage in breast cancer cells was further accelerated by combination with Mag. DOX-induced cell distribution in G2/M phase was markedly elevated when co-treated with Mag. Additionally, DOX/Mag combinational treatment significantly induced apoptosis in breast cancer cells when compared to DOX alone group through inducing Caspase-3 cleavage. Moreover, Mag markedly promoted the role of DOX in autophagy induction by elevating light chain 3 (LC3)-II expression. Combination treatment with DOX and Mag significantly inhibited the activation of phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling, and promoted p38 mitogen-activated protein kinase (MAPK) pathway. In addition, treatment with wortmannin (Wor, a blocker of autophagosome formation) markedly reduced DOX/Mag-induced p38 MAPK activation and LC3 conversion in breast cancer cells. Further, in MCF-7 xenograft model, DOX combined with Mag displayed a significant anti-tumor effect with little toxicity to organs such as liver, heart, kidney and spleen. These findings suggested that Mag promoted the anti-cancer effects of DOX to induce cellular apoptosis and autophagy in breast cancer cells.
Magnoflorine Attenuates Cerebral Ischemia-Induced Neuronal Injury via Autophagy/Sirt1/AMPK Signaling Pathway
Evid Based Complement Alternat Med 2022 Sep 10;2022:2131561.PMID:36124014DOI:10.1155/2022/2131561.
Ischemic stroke is a common cause of permanent disability worldwide. Magnoflorine has been discovered to have good antioxidation, immune regulation, and cardiovascular system protection functions. However, whether Magnoflorine treatment protects against cerebral ischemic stroke and the mechanism of such protection remains unknown. Here, we investigated the effect of Magnoflorine on the development of ischemic stroke disorder in rats. A middle cerebral artery occlusion (MCAO) model followed by 24 h reperfusion after 90 min ischemia was used. The rats were treated with Magnoflorine (10 mg/kg or 20 mg/kg) for 15 consecutive days. The neurological deficit scores, cerebral infarct volume, and brain water content were measured. The neuronal density was determined using Nissl and NeuN staining. The oxidative stress levels were determined using commercial kits. Immunofluorescence staining of LC3 and western blot assay for LC3 and p62 were used to assess autophagy. Magnoflorine treatment significantly reduced the cerebral infarct volume and brain water content and improved the neurological deficit scores in the rat MCAO model. In addition, Magnoflorine ameliorated neuronal injury and neuron density in the cortex of rats. Magnoflorine also prevented oxidative damage following ischemia, reflected by the decrement of nitric oxide and malondialdehyde and the increase of glutathione (GSH) and GSH peroxidase. Moreover, the fluorescence intensity of LC3 and the ratio of LC3-II to LC3-I were remarkably downregulated in ischemic rat administration of Magnoflorine. Finally, the expression levels of p62, sirtuin 1 (Sirt1), and phosphorylated-adenosine monophosphate-activated protein kinase (AMPK) were upregulated with Magnoflorine. Magnoflorine attenuated the cerebral ischemia-induced neuronal damage, which was possibly associated with antioxidative stress, suppression of autophagy, and activation of the Sirt1/AMPK pathway in the rats.
Magnoflorine Alleviates "M1" Polarized Macrophage-Induced Intervertebral Disc Degeneration Through Repressing the HMGB1/Myd88/NF-κB Pathway and NLRP3 Inflammasome
Front Pharmacol 2021 Jul 23;12:701087.PMID:34366853DOI:10.3389/fphar.2021.701087.
Intervertebral disc degeneration (IDD) is related to the deterioration of nucleus pulposus (NP) cells due to hypertrophic differentiation and calcification. The imbalance of pro-inflammatory (M1 type) and anti-inflammatory (M2 type) macrophages contributes to maintaining tissue integrity. Here, we aimed to probe the effect of Magnoflorine (MAG) on NP cell apoptosis mediated by "M1" polarized macrophages. THP-1 cells were treated with lipopolysaccharide (LPS) to induce "M1" polarized macrophages. Under the treatment with increasing concentrations of MAG, the expression of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α, IL-18), high mobility group box protein 1 (HMGB1), as well as myeloid differentiation factor 88 (MyD88), nuclear factor kappa B (NF-κB) and NOD-like receptor 3 (NLRP3) inflammasomes in THP-1 cells were determined. What's more, human NP cells were treated with the conditioned medium (CM) from THP-1 cells. The NP cell viability and apoptosis were evaluated. Western blot (WB) was adopted to monitor the expression of apoptosis-related proteins (Bax, Caspase3, and Caspase9), catabolic enzymes (MMP-3, MMP-13, ADAMTS-4, and ADAMTS-5), and extracellular matrix (ECM) compositions (collagen II and aggrecan) in NP cells. As a result, LPS evidently promoted the expression of pro-inflammatory cytokines and HMGB1, the MyD88-NF-κB activation, and the NLRP3 inflammasome profile in THP-1 cells, while MAG obviously inhibited the "M1″ polarization of THP-1 cells. After treatment with "M1" polarized THP-1 cell CM, NP cell viability was decreased, while cell apoptosis, the pro-inflammatory cytokines, apoptosis-related proteins, and catabolic enzymes were distinctly up-regulated, and ECM compositions were reduced. After treatment with MAG, NP cell damages were dramatically eased. Furthermore, MAG dampened the HMGB1 expression and inactivated the MyD88/NF-κB pathway and NLRP3 inflammasome in NP cells. In conclusion, this study confirmed that MAG alleviates "M1" polarized macrophage-mediated NP cell damage by inactivating the HMGB1-MyD88-NF-κB pathway and NLRP3 inflammasome, which provides a new reference for IDD treatment.