α-Mangostin (α-Mangostin) 抑制 IDH1-R132H，但不抑制 IDH1。 IDH1-R132H 受 α-Mangostin (α-Mangostin) 抑制。根据研究，最强的核心翻转结构出现在α-山竹素（α-Mangostin）中。 α-Mangostin (α-Mangostin) 优先刺激 IDH1 (+/R132H) MCF10A 细胞中组蛋白 H3 和 5-甲基纤维素 (5mC) 中三甲基化赖氨酸残基的去甲基化 [1]。在用 α-倒挂素处理的细胞中，细胞增殖受到显着且剂量依赖性的抑制。此外，α-山竹还能提高线粒体 caspase-9、线粒体 caspase-3、线粒体聚（ADP-核糖）聚合酶 (PARP) 和色素原 Bax 水平 [2]。 α-山竹素 (α-Mangostin) 显着降低光引起的活性氧 (ROS) 和丙二醛 (MDA) 的产生，在 200 μM H2O2 下，α-山竹素 (α-Mangostin) 会抑制光引起的活性氧 (ROS) 和丙二醛 (MDA) 的产生[3]。

与 TAA_DMSO 疗法相比，α-Mangostin (α-Mangostin) 降低了 p53 表达，从而降低了肝纤维化的风险。与单独使用 DMSO 相比，α-Mangostin 治疗可降低血清中肝酶 AST 和 ALT 的水平 [4]。

Interactions
Altered membrane integrity and inflammation play a key role in cardiovascular damage. /The authors/ investigated the salubrious effect of exogenously administered alpha-mangostin against beta-adrenergic cathecolamine-induced cardiovascular toxicity with special reference to membrane ATPases, lysosomal hydrolases and inflammatory mediators TNF-alpha and Cyclooxygenase-2 (COX-2) expressions in albino rats. Induction of rats with isoproterenol (150 mg/kg body wt, ip) for 2 days resulted in a significant increase in the activities of serum and cardiac lysosomal hydrolases (beta-d-glucuronidase, beta-d-galactosidase, beta-d-N-acetylglucosaminidase, acid phosphatase and cathepsin-D). A significant increase in cardiac levels of sodium, calcium with a decrease in the level of potassium paralleled by abnormal activities of membrane-bound phosphatases (Na(+)-K(+) ATPase, Ca(2+) ATPase and Mg(2+) ATPase) were observed in the heart of ISO-administered rats. Cardiac TNF-alpha and COX-2 expressions were assessed by Western blotting. Cardiac TNF-alpha and COX-2 expressions were significantly elevated in ISO-intoxicated rats. Pre-co-treatment with alpha-mangostin (200mg/kg body wt.) orally for 8 days significantly attenuated these abnormalities and restored the levels to near normalcy when compared to ISO intoxicated group of rats. In conclusion, alpha-mangostin preserves the myocardial membrane integrity and extenuates anomalous TNF-alpha and COX-2 expressions by mitigating ISO-induced oxidative stress and cellular damage effectively. Restoration of cellular normalcy accredits the cytoprotective role of alpha-mangostin.
Cisplatin (CDDP) is a chemotherapeutic agent that produces nephrotoxicity associated with oxidative/nitrosative stress. alpha-Mangostin (alpha-M) is a xanthone extracted from mangosteen with antioxidant and anti-inflammatory properties. The purpose of this study was to evaluate the renoprotective effect of alpha-M on the CDDP-induced nephrotoxicity. alpha-M was administered (12.5 mg/kg/day, i.g.) for 10 days (7 days before and 3 days after CDDP injection). On day 7, rats were treated with a single injection of CDDP (7.5 mg/Kg, i.p.); 3 days after the rats were killed. alpha-M attenuated renal dysfunction, structural damage, oxidative/nitrosative stress, decrease in catalase expression and increase in mRNA levels of tumour necrosis factor alpha and transforming growth factor beta. In conclusion the renoprotective effect of alpha-M on CDDP-induced nephrotoxicity was associated with the attenuation in oxidative/nitrosative stress and inflammatory and fibrotic markers and preservation of catalase activity.
alpha-Mangostin, isolated from the stem bark of Garcinia mangostana L., was found to be active against vancomycin resistant Enterococci (VRE) and methicillin resistant Staphylococcus aureus (MRSA), with minimum inhibitory concentration (MIC) values of 6.25 and 6.25 to 12.5 ug/mL, respectively. Our studies showed synergism between alpha-mangostin and gentamicin (GM) against VRE, and alpha-mangostin and vancomycin hydrochloride (VCM) against MRSA. Further studies showed partial synergism between alpha-mangostin and commercially available antibiotics such as ampicillin and minocycline. These findings suggested that alpha-mangostin alone or in combination with GM against VRE and in combination with VCM against MRSA might be useful in controlling VRE and MRSA infections.

[1]. Discovery of α-mangostin as a novel competitive inhibitor against mutant isocitrate dehydrogenase-1. Bioorg Med Chem Lett. 2015 Dec 1;25(23):5625-31.

[2]. Antitumor and apoptosis-inducing effects of α-mangostin extracted from the pericarp of the mangosteen fruit (Garcinia mangostana L.) in YD-15 tongue mucoepidermoid carcinoma cells. Int J Mol Med. 2016 Apr;37(4):939-48.

Alpha-mangostin is a member of the class of xanthones that is 9H-xanthene substituted by hydroxy group at positions 1, 3 and 6, a methoxy group at position 7, an oxo group at position 9 and prenyl groups at positions 2 and 8. Isolated from the stems of Cratoxylum cochinchinense, it exhibits antioxidant, antimicrobial and antitumour activities. It has a role as an antineoplastic agent, an antimicrobial agent, an antioxidant and a plant metabolite. It is a member of xanthones, a member of phenols and an aromatic ether.
Mangostin is a plant/plant extract used in some OTC (over-the-counter) products. It is not an approved drug.
alpha-Mangostin has been reported in Garcinia cowa, Garcinia merguensis, and other organisms with data available.
See also: Garcinia mangostana fruit rind (part of).

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Therapeutic Uses
*Xanthones; Protein Kinase Inhibitors
/EXPERIMENTAL THERAPY/The mangosteen fruit has a long history of medicinal use in Chinese and Ayurvedic medicine. Recently, the compound a-mangostin, which is isolated from the pericarp of the fruit, was shown to induce cell death in various types of cancer cells in in vitro studies. This led us to investigate the antitumor growth and antimetastatic activities of a-mangostin in an immunocompetent xenograft model of mouse metastatic mammary cancer having a p53 mutation that induces a metastatic spectrum similar to that seen in human breast cancers. Mammary tumors, induced by inoculation of BALB/c mice syngeneic with metastatic BJMC3879luc2 cells, were subsequently treated with a-mangostin at 0, 10 and 20 mg/kg/day using mini-osmotic pumps and histopathologically examined. To investigate the mechanisms of antitumor ability by a-mangostin, in vitro studies were also conducted. Not only were in vivo survival rates significantly higher in the 20 mg/kg/day a-mangostin group versus controls, but both tumor volume and the multiplicity of lymph node metastases were significantly suppressed. Apoptotic levels were significantly increased in the mammary tumors of mice receiving 20 mg/kg/day and were associated with increased expression of active caspase-3 and -9. Other significant effects noted at this dose level were decreased microvessel density and lower numbers of dilated lymphatic vessels containing intraluminal tumor cells in mammary carcinoma tissues. In vitro, a-mangostin induced mitochondria-mediated apoptosis and G1-phase arrest and S-phase suppression in the cell cycle. Since activation by Akt phosphorylation plays a central role in a variety of oncogenic processes, including cell proliferation, anti-apoptotic cell death, angiogenesis and metastasis, we also investigated alterations in Akt phosphorylation induced by a-mangostin treatment both in vitro and in vivo. Quantitative analysis and immunohistochemistry showed that a-mangostin significantly decreased the levels of phospho-Akt-threonine 308 (Thr308), but not serine 473 (Ser473), in both mammary carcinoma cell cultures and mammary carcinoma tissues in vivo. Since lymph node involvement is the most important prognostic factor in breast cancer patients, the antimetastatic activity of a-mangostin as detected in mammary cancers carrying a p53 mutation in the present study may have specific clinical applications. In addition, a-mangostin may have chemopreventive benefits and/or prove useful as an adjuvant therapy, or as a complementary alternative medicine in the treatment of breast cancer.
/EXPERIMENTAL THERAPY/This study was conducted to examine the activity of alpha-mangostin against Candida albicans, the most important microorganism implicated in oral candidiasis. Its activity was compared to Clotrimazole and Nystatin. Results showed that alpha-mangostin was effective against C. albicans, the minimum inhibitory concentration (MIC) and minimum fungicidal concentration (MFC) were 1,000 and 2,000 ug/mL, respectively. The C. albicans killing activity of alpha-mangostin was more effective than Clotrimazole and Nystatin. The cytotoxicity of alpha-mangostin was determined and it was found that alpha-mangostin at 4,000 ug/mL was not toxic to human gingival fibroblast for 480 min. The strong antifungal activity and low toxicity of alpha-mangostin make it a promising agent for treatment of oral candidiasis.
/EXPERIMENTAL THERAPY/ Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by the accumulation of beta-sheet-rich amyloid oligomers or fibrils which are associated with cellular toxicity in the brain. Inhibition of Abeta aggregation could be a viable therapeutic strategy for slowing and/or preventing the progress of AD. Here /the authors/ reported that a-mangostin (a-M), a polyphenolic xanthone derivative from mangosteen, concentration-dependently attenuated the neurotoxicity induced by Abeta-(1-40) or Abeta-(1-42) oligomers (EC(50) = 3.89 nM, 4.14 nM respectively) as observed by decreased cell viability and impaired neurite outgrowth in primary rat cerebral cortical neurons. Molecular docking and dynamics simulations demonstrated that a-M could potentially bind to Abeta and stabilize alpha-helical conformation. a-M was found to directly dissociate Abeta-(1-40) and Abeta-(1-42) oligomers by blotting with oligomer-specific antibodies. ThioflavinT fluorescence assay and electron microscopy imaging further demonstrated that a-M blocked the fibril formation as well as disturbed the pre-formed fibrils. Taken together, /these/ results indicate that a-M is capable /of/ inhibiting and dissociating the Abeta aggregation, which could contribute to its effect of attenuating Abeta oligomers-induced neurotoxicity. Thus, a-M could be a great potential candidate for AD treatment...

C24H26O6

410.4596

410.172

C, 70.23; H, 6.38; O, 23.39

6147-11-1

beta-Mangostin; 20931-37-7

5281650

Yellow solid solid

1.3±0.1 g/cm3

640.1±55.0 °C at 760 mmHg

182ºC

220.3±25.0 °C

0.0±2.0 mmHg at 25°C

1.624

5.45

100.13

3

6

5

30

677

0

O1C2C([H])=C(C(C([H])([H])/C(/[H])=C(\C([H])([H])[H])/C([H])([H])[H])=C(C=2C(C2=C1C([H])=C(C(=C2C([H])([H])/C(/[H])=C(\C([H])([H])[H])/C([H])([H])[H])OC([H])([H])[H])O[H])=O)O[H])O[H]

GNRIZKKCNOBBMO-UHFFFAOYSA-N

InChI=1S/C24H26O6/c1-12(2)6-8-14-16(25)10-19-21(22(14)27)23(28)20-15(9-7-13(3)4)24(29-5)17(26)11-18(20)30-19/h6-7,10-11,25-27H,8-9H2,1-5H3

1,3,6-trihydroxy-7-methoxy-2,8-bis(3-methylbut-2-enyl)xanthen-9-one

NSC 27593; NSC 139154; NSC 30552; Alpha-Mangostin; NSC27593; NSC139154; NSC30552

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 : ~110 mg/mL (~267.99 mM)
H2O : < 0.1 mg/mL

配方 1 中的溶解度: ≥ 2.75 mg/mL (6.70 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 27.5 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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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。