(S)-Equol
(Synonyms: 雌马酚) 目录号 : GC49520
(S)-Equol是一种由部分人群肠道微生物产生的异黄烷类化合物，主要来源于大豆中的大豆素在特定肠道菌群的作用下生成。(S)-Equol具有显著的雌激素样活性和抗氧化特性，能够与雌激素受体结合，对 ERβ的亲和力为Ki=0.73±0.2nM，对ERα的亲和力为Ki=6.41±1nM。
Cas No.:531-95-3
Sample solution is provided at 25 µL, 10mM.
(S)-Equol is an isoflavone compound produced by the gut microbiota of some individuals, primarily derived from the metabolism of daidzein in soybeans by specific gut bacteria[1]. (S)-Equol exhibits significant estrogenic activity and antioxidant properties, binding to estrogen receptors with an affinity for ERβ of Ki=0.73±0.2nM and for ERα of Ki=6.41±1nM[2]. (S)-Equol also has antioxidant effects, scavenging free radicals in the body to reduce oxidative stress and prevent the development of cardiovascular diseases and certain chronic conditions[3]. (S)-Equol has demonstrated antitumor activity by regulating the cell cycle and inducing apoptosis, inhibiting tumor cell growth and spread, and providing new insights for cancer prevention and adjuvant therapy[4].
In vitro, 30μM (S)-Equol pre-treatment of rat primary chondrocytes for 24h, followed by stimulation with 0.8mM Sodium nitroprusside (SNP; 50μM) for 24h, significantly activated the PI3K/Akt signaling pathway, reducing SNP-induced cell death, oxidative stress, apoptosis, and proteoglycan loss, while inhibiting the expression of matrix metalloproteinases (MMPs) and p53[5]. 0.1-10μM (S)-Equol pre-treatment of rat insulinoma beta cell line INS-1 cells, followed by stimulation with high glucose (26.2mM) for 48h, significantly enhanced insulin secretion, decreased cell apoptosis, and inhibited the Chrebp/Txnip signaling pathway, activating PKA/PP2A activity[6].
In vivo, (S)-Equol (20, 40, 80mg/kg) administered daily via gavage for 12 weeks in a diabetic osteoporosis (DOP) rat model significantly increased bone density, improved bone microstructure, and enhanced bone formation markers while reducing bone resorption markers, ameliorating DOP[7]. (S)-Equol (2mg/kg/d) administered orally daily for 8 weeks in a Sprague–Dawley (SD) rat model of varying degrees of menopausal osteoarthritis (OA) significantly reduced OA pathological damage, oxidative stress, and cartilage matrix degradation[8].
References:
[1] Chen LR, Chen KH. Utilization of Isoflavones in Soybeans for Women with Menopausal Syndrome: An Overview. Int J Mol Sci. 2021 Mar 22;22(6):3212.
[2] Setchell KD, Clerici C, Lephart ED, et al. S-equol, a potent ligand for estrogen receptor beta, is the exclusive enantiomeric form of the soy isoflavone metabolite produced by human intestinal bacterial flora. Am J Clin Nutr. 2005 May;81(5):1072-9.
[3] Sekikawa A, Wharton W, Butts B, et al. Potential Protective Mechanisms of S-equol, a Metabolite of Soy Isoflavone by the Gut Microbiome, on Cognitive Decline and Dementia. Int J Mol Sci. 2022 Oct 7;23(19):11921.
[4] Zhang J, Ren L, Yu M, et al. S-equol inhibits proliferation and promotes apoptosis of human breast cancer MCF-7 cells via regulating miR-10a-5p and PI3K/AKT pathway. Arch Biochem Biophys. 2019 Sep 15;672:108064.
[5] Huang LW, Huang TC, Hu YC, et al. S-Equol Protects Chondrocytes against Sodium Nitroprusside-Caused Matrix Loss and Apoptosis through Activating PI3K/Akt Pathway. Int J Mol Sci. 2021 Jun 30;22(13):7054.
[6] Chen K, Lang H, Wang L, et al. S-Equol ameliorates insulin secretion failure through Chrebp/Txnip signaling via modulating PKA/PP2A activities. Nutr Metab (Lond). 2020 Jan 14;17:7.
[7] Xu Z, Xu J, Li S, et al. S-Equol enhances osteoblastic bone formation and prevents bone loss through OPG/RANKL via the PI3K/Akt pathway in streptozotocin-induced diabetic rats. Front Nutr. 2022 Oct 21;9:986192.
[8] Hu YC, Huang TC, Huang LW, et al. S-Equol Ameliorates Menopausal Osteoarthritis in Rats through Reducing Oxidative Stress and Cartilage Degradation. Nutrients. 2024 Jul 21;16(14):2364.
(S)-Equol是一种由部分人群肠道微生物产生的异黄烷类化合物，主要来源于大豆中的大豆素在特定肠道菌群的作用下生成[1]。(S)-Equol具有显著的雌激素样活性和抗氧化特性，能够与雌激素受体结合，对ERβ的亲和力为Ki=0.73±0.2nM，对ERα的亲和力为Ki=6.41±1nM[2]。(S)-Equol还具有抗氧化作用，可以清除体内自由基，减少氧化应激损伤，对心血管疾病和某些慢性疾病的发生发展具有一定的预防作用[3]。(S)-Equol还表现出一定的抗肿瘤活性，能够通过调节细胞周期和诱导细胞凋亡等方式，抑制肿瘤细胞的生长和扩散，为癌症的预防和辅助治疗提供了新的思路[4]。
在体外，30μM (S)-Equol预处理大鼠原代软骨细胞24h，随后以0.8mM Sodium nitroprusside（SNP；50μM）刺激24h，(S)-Equol显著激活PI3K/Akt信号通路，减轻SNP诱导的细胞死亡、氧化应激、凋亡以及蛋白多糖丢失，同时抑制基质金属蛋白酶（MMPs）及p53的表达[5]。0.1-10μM (S)-Equol预处理大鼠胰岛β细胞系INS-1细胞，随后以高葡萄糖（26.2mM）刺激48h，(S)-Equol显著增强胰岛素分泌，降低细胞凋亡，同时抑制Chrebp/Txnip信号通路，激活PKA/PP2A活性[6]。
在体内，(S)-Equol（20、40、80mg/kg）每日一次灌胃处理，用于干预糖尿病性骨质疏松症（DOP）大鼠模型12周。(S)-Equol显著提高了大鼠的骨密度，改善了骨微结构，增加了骨形成标志物水平，降低了骨吸收标志物水平，改善DOP[7]。S-Equol（2mg/kg/d）每日一次口服给药，用于干预不同程度绝经后骨关节炎（OA）Sprague–Dawley（SD）大鼠模型8周。S-Equol显著减轻了大鼠模型的骨关节炎病理损伤、氧化应激和软骨基质降解[8]。
| Cell experiment [1]: | |
Cell lines | INS-1 cells (rat insulinoma beta cells) |
Preparation Method | INS-1 cells were cultured in RPMI 1640 medium containing 10% fetal bovine serum (FBS), 1% penicillin/streptomycin, 1mM sodium pyruvate, 2mM L-glutamine, 10mM HEPES, and 0.05mM 2-mercaptoethanol at 37°C, 5% CO₂. Cells were treated with (S)-Equol (0.1μM, 1μM, 10μM) in the presence of high glucose (26.2mM) for 48 hours. |
Reaction Conditions | 0.1-10μM; 48 hours |
Applications | (S)-Equol treatment enhanced glucose-stimulated insulin secretion (GSIS) in high glucose-cultured INS-1 cells. (S)-Equol also reduced cell apoptosis, as evidenced by decreased apoptotic cell numbers. (S)-Equol significantly increased the expression of preproinsulin (PPI) mRNA and Glut2 protein, while decreasing UCP-2 protein levels. |
| Animal experiment [2]: | |
Animal models | Sprague–Dawley (SD) rats |
Preparation Method | Rats were subjected to bilateral ovariectomy (OVX) to induce estrogen deficiency and intra-articular injection of mono-iodoacetate (MIA) to induce osteoarthritis (OA). Rats were divided into sham, OVX, OVX with low-dose MIA (0.1mg), and OVX with high-dose MIA (1mg) groups. (S)-Equol (2mg/kg/d) was administered orally for 8 weeks. |
Dosage form | 2mg/kg/d; oral administration |
Applications | (S)-Equol supplementation significantly reduced body weight gain, serum triglyceride levels, and oxidative stress markers. (S)-Equol also decreased cartilage degradation biomarkers, matrix-degrading enzymes, and improved histopathological changes in the knee joint, indicating its potential to mitigate menopausal OA progression. |
References: | |
| Cas No. | 531-95-3 | SDF | Download SDF |
| 别名 | 雌马酚 | ||
| Canonical SMILES | OC1=CC=C2C(OC[C@H](C3=CC=C(O)C=C3)C2)=C1 | ||
| 分子式 | C15H14O3 | 分子量 | 242.3 |
| 溶解度 | DMF: 15 mg/ml,DMSO: 20 mg/ml,Ethanol: 20 mg/ml,Ethanol:PBS (pH 7.2) (1:10): 0.1 mg/ml | 储存条件 | -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 | 4.1271 mL | 20.6356 mL | 41.2712 mL |
| 5 mM | 825.4 μL | 4.1271 mL | 8.2542 mL |
| 10 mM | 412.7 μL | 2.0636 mL | 4.1271 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，
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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。
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