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(Synonyms: 氯化缬草素) 目录号 : GC60378

Valechlorine,一种自噬增强剂,可分解脂滴。Valechlorine 以 Atg5 依赖性方式减少油酸 (OA) 诱导的脂质蓄积。

Valechlorine Chemical Structure

Cas No.:51771-49-4

规格 价格 库存
5mg
¥990.00
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10mg
¥1,710.00
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25mg
¥3,060.00
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Sample solution is provided at 25 µL, 10mM.

产品文档

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产品描述

Valechlorine, a autophagy enhancer, breaks down lipid droplets. Valechlorine reduces oleic acid (OA)-induced lipid accumulation in an Atg5-dependent manner[1].

[1]. Lee DH, et al. Iridoids of Valeriana fauriei contribute to alleviating hepatic steatosis in obese mice by lipophagy.Biomed Pharmacother. 2020 Feb 10;125:109950.

Chemical Properties

Cas No. 51771-49-4 SDF
别名 氯化缬草素
Canonical SMILES O[C@]1(CCl)[C@@H](OC(CC(C)C)=O)C=C2[C@]1([H])[C@H](OC(CC(C)C)=O)OC=C2COC(C)=O
分子式 C22H31ClO8 分子量 458.93
溶解度 储存条件
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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。

溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.179 mL 10.8949 mL 21.7898 mL
5 mM 0.4358 mL 2.179 mL 4.358 mL
10 mM 0.2179 mL 1.0895 mL 2.179 mL
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Research Update

Iridoids of Valeriana fauriei contribute to alleviating hepatic steatosis in obese mice by lipophagy

Biomed Pharmacother 2020 May;125:109950.PMID:32058217DOI:10.1016/j.biopha.2020.109950

Nonalcoholic fatty liver disease (NAFLD) is a common risk factor for metabolic syndrome that increases the risk of future cardiovascular disease, stroke, and diabetes. Recently, autophagy has been proposed as a means to prevent NAFLD. We investigated whether substances with autophagy-inducing activity alleviate NAFLD. The Valeriana fauriei (V. fauriei) was selected as a potential autophagy inducer among various natural materials using a Cyto-ID autophagy detection kit. V. fauriei 70 % ethanol extract (VFE) increased LC3II levels in the presence of the lysosomal inhibitor and reduced the GFP/mCherry puncta ratio, suggesting that VFE enhanced autophagy. VFE reduced oleic acid (OA)-induced lipid accumulation and increased the number of autophagosome in hepatocytes. Autophagy induction by VFE is due to inhibition of mTORC1 activity. VFE supplementation reduced fatty liver by downregulating lipogenesis-related genes and increased the autophagy, as revealed by TEM and IHC analysis in the fatty liver. We identified iridoids as main compounds of VFE; didrovaltrate (DI), valeriotriate B (VAL B), valeriotetrate C (VAL C), valtrate (VAL), and Valechlorine (VC) were shown to enhance autophagy. These compounds also reduced OA-induced lipid accumulation in an Atg5-dependent manner. Taken together, VFE and its iridoids might be effective in alleviating fatty liver by acting as autophagy enhancers to break down LDs.