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Toringin Sale

(Synonyms: 三叶海棠素) 目录号 : GC37816

Toringin,是一种从 Docyniopsis tschonoski 的树皮中分离出来的生物类黄酮。 Toringin 不仅逐渐降低扩增的 CTG 重复顺式效应,而且还降低细胞毒性。 暴露于异樱花素 (isosakuranetin),Toringin 保护 PC12 神经细胞。 类黄酮化合物能够改善由扩增的 CTG 重复引起的功能RNA增加,并且对癌症,冠心病以及其他病症产生有益的作用。

Toringin Chemical Structure

Cas No.:1329-10-8

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5mg
¥2,727.00
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产品描述

Toringin, a bioflavonoid, is isolated from the bark of Docyniopsis tschonoski. Toringin progressively decreases not only the cis-effect of the expanded CTG repeats but cytotoxicity as well. Exposure to isosakuranetin, Toringin rescues PC12 neuronal cells. Flavonoids are efficacious for ameliorating the RNA gain of function caused by expanded CTG repeats, and have various biological activities and beneficial actions against cancers, coronary heart disease, among other pathologies[1].

[1]. Furuya H, et al. Some flavonoids and DHEA-S prevent the cis-effect of expanded CTG repeats in a stable PC12 cell transformant. Biochem Pharmacol. 2005 Feb 1;69(3):503-16.

Chemical Properties

Cas No. 1329-10-8 SDF
别名 三叶海棠素
Canonical SMILES O=C1C(C(OC(C2=CC=CC=C2)=C1)=CC(O)=C3)=C3O[C@@H]4O[C@@H]([C@@H](O)[C@H](O)[C@H]4O)CO
分子式 C21H20O9 分子量 416.38
溶解度 Soluble in DMSO 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 2.4017 mL 12.0083 mL 24.0165 mL
5 mM 0.4803 mL 2.4017 mL 4.8033 mL
10 mM 0.2402 mL 1.2008 mL 2.4017 mL
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Research Update

Some flavonoids and DHEA-S prevent the cis-effect of expanded CTG repeats in a stable PC12 cell transformant

Biochem Pharmacol 2005 Feb 1;69(3):503-16.PMID:15652241DOI:10.1016/j.bcp.2004.10.005

Expanded CUG triplet repeats carrying mRNA seem to be responsible for myotonic dystrophy type 1 (DM1). To study the pathogenesis of DM1, we constructed a DM1 cell culture model using a PC12 neuronal cell line and screened flavonoids that ameliorate this mRNA gain of function. The expanded 250 CTG repeat was subcloned into the 3'-untranslated region of the luciferase gene yielding a stable transformant of PC12 (CTG-250). The cytotoxicity of CTG-250 was evaluated by intracellular LDH activity, and the cis-effect by luciferase activity. To find agents that alter CTG-250 toxic effects, 235 bioflavonoids were screened. An increased cis-effect and cytotoxicity were found when CTG-250 was treated with nerve growth factor to induce differentiation. Western blotting with anti-caspase-3 antibody suggested that cell death was caused by apoptosis. Screening analysis confirmed that a flavone (Toringin), an isoflavones (genistein and formononetin), a flavanone (isosakuranetin), and DHEA-S prevent both the cytotoxicity and cis-effect of CTG-250 and that a flavanone (naringenin), isoflavone (ononin), and xanthylatin strongly inhibit the cis-effect of CTG repeats. In conclusion, we found that this neuronal cell line, which expresses the CUG repeat-bearing mRNA, showed cis-effects through the reporter gene and neuronal death after cell differentiation in vitro. However, some flavonoids and DHEA-S inhibit both the cis-effect and cytotoxicity, indicating that their chemical structures work to ameliorate both these toxic effects. This system makes it easy to evaluate the toxic effects of expanded CTG repeats and therefore should be useful for screening other DM1 treatments for their efficacies.