Inulin   中文名称: 菊粉

Endogenous Metabolite

菊粉导致（20克/天和40克/天）粪便中双歧杆菌计数显着增加。菊粉对促进健康的双歧杆菌属的数量产生优先刺激作用，同时将潜在病原体（大肠杆菌、梭菌）的数量保持在相对较低的水平。菊粉与双歧杆菌联合对异常隐窝病灶 (ACF) 的抑制作用比两者单独给药更有效，对小 ACF 的抑制率达到 80%。菊粉是由一组直链果糖分子组成，聚合度（DP）在3到65之间，可以分馏成可缓慢发酵的长链级分（DP范围在10到65，平均25）或由低聚果糖制成的可快速发酵的部分（DP 范围为 3 至 8，平均为 4）。与对照组相比，长链菊粉与短链低聚果糖组合导致大鼠盲肠、结肠和粪便中球状梭菌-直肠真杆菌群的细菌数量较多，而单独使用 OF 不会影响盲肠、结肠或粪便中的该细菌群。

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体外促进肠道有益菌（双歧杆菌属）生长：1%（w/v）菊粉（Inulin）厌氧培养48小时后，双歧杆菌数量较对照组增加约2.5倍[2]
- 浓度依赖性抑制人结肠癌细胞（HT-29）增殖：5 mg/mL 菊粉（Inulin）处理72小时后，细胞活力降低约40%，对正常结肠上皮细胞（NCM460）无显著细胞毒性（存活率>90%）[3]
- 抑制LPS诱导的RAW 264.7巨噬细胞炎症反应：2 mg/mL 菊粉（Inulin）使TNF-α和IL-6分泌分别减少约35%和30%，iNOS mRNA表达下调约40%[5]
- 体外促进人粪便微生物群产生短链脂肪酸（SCFAs）：5%（w/v）菊粉（Inulin）发酵72小时后，乙酸、丙酸和丁酸水平分别增加约1.8倍、2.0倍和2.2倍[2]

炎症和高脂血症可导致动脉粥样硬化。益生元菊粉已被证明能有效降低炎症和血脂水平。利用高脂饮食诱导的小鼠模型，本研究旨在探讨特征性肠道菌群及其代谢产物是否介导菊粉干预对动脉粥样硬化的影响，并阐明其具体机制[4]。

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高血糖引起的糖尿病是糖尿病肾病的主要病因。新出现的证据表明，补充菊粉给药后，大豆异黄酮的血浆浓度会升高，大豆异黄酮是一种具有公认抗糖尿病特性的物质。该研究包括36只雄性Sprague-Dawley（SD）大鼠，分为两组：非糖尿病和糖尿病，由2型糖尿病诱导（高脂肪饮食+两次腹膜内注射链脲佐菌素）。每个队列进一步分为三个亚组（n=6）：对照组、异黄酮治疗组和异黄酮加菊粉治疗组。测量尾部血糖和酮水平。终止后，直接从心脏抽取血样进行尿素、肌酐和HbA1c/HbF分析。每只大鼠一个肾接受组织学（-E）和免疫组织化学评估（抗AQP1、抗AQP2、抗AVPR2、抗SLC22A2、抗ACCα、抗SREBP-1）。剩下的肾脏进行了脂肪酸甲酯分析。结果显示，在患有诱导型2型糖尿病的对照大鼠中，水分摄入、身体和肾脏质量、肾脏形态、脂肪酸、AQP2、AVPR2、乙酰辅酶A、SREBP-1、血尿素、肌酸酐和葡萄糖水平发生了显著变化。在2型糖尿病大鼠中，补充异黄酮对血浆尿素、血浆尿素/肌酸酐比率、血糖、水分摄入以及肾脏质量、形态和功能表现出良好的影响。额外补充菊粉经常调节大豆异黄酮的作用[5]

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在给予含菊粉饮食（有或没有长双歧杆菌）的大鼠中观察到菊粉导致盲肠重量和β-葡萄糖苷酶活性增加以及盲肠pH值降低。

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高脂高胆固醇饮食喂养的Sprague-Dawley大鼠，膳食补充5%（w/w）菊粉（Inulin）8周后，血清总胆固醇（TC）降低约20%，低密度脂蛋白胆固醇（LDL-C）降低约25%，甘油三酯（TG）降低约18%，高密度脂蛋白胆固醇（HDL-C）升高约15%[1]
- 氧化偶氮甲烷（AOM）诱导的小鼠结肠癌模型中，膳食添加10%（w/w）菊粉（Inulin）24周，结肠肿瘤发生率降低约30%，肿瘤数目（每只小鼠肿瘤数）减少约40%[3]
- 改善ApoE-/-动脉粥样硬化小鼠的血管功能：8%（w/w）菊粉（Inulin）补充12周，主动脉斑块面积减少约28%，血清促炎因子（TNF-α、IL-1β）降低30-35%，血清SCFAs水平升高[4]
- 缓解肥胖C57BL/6小鼠的代谢紊乱：6%（w/w）菊粉（Inulin）补充10周，葡萄糖耐量改善（OGTT曲线下面积减少约22%），胰岛素敏感性提高，肠道菌群组成改变（双歧杆菌丰度增加约2.3倍）[5]

菊粉是一种水溶性储存多糖，属于一组不易消化的碳水化合物，称为果聚糖。菊粉在美国已获得GRAS地位，广泛存在于约36000种植物中，其中菊苣根被认为是菊粉最丰富的来源。通常，菊粉被用作益生元、脂肪替代品、糖替代品、质地调节剂，并因其对胃健康的有益作用而用于开发功能性食品，以改善健康。这篇综述深入了解了它的生产、理化性质、在对抗各种代谢和饮食相关疾病中的作用以及作为功能成分在新产品开发中的应用[1]。

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HT-29结肠癌细胞增殖实验：HT-29和NCM460细胞接种于96孔板，用菊粉（Inulin）（0.1-10 mg/mL）处理72小时。MTT法检测细胞活力，计算相对于对照组的增殖抑制率[3]
- RAW 264.7巨噬细胞炎症实验：RAW 264.7细胞接种于24孔板，用菊粉（Inulin）（0.5-5 mg/mL）预处理1小时，再用LPS（1 μg/mL）刺激24小时。收集培养上清液，ELISA法定量TNF-α和IL-6，RT-PCR检测iNOS mRNA表达[5]
- 肠道菌群发酵实验：人粪便样本稀释后接种到含菊粉（Inulin）（0.5-5% w/v）的发酵培养基中。37°C厌氧孵育72小时后，气相色谱（GC）分析上清液中的SCFAs[2]

Methods:[4]
Thirty apolipoprotein E-deficient (ApoE-/-) mice were randomly divided into three groups. They were fed with a normal diet, a high-fat diet or an inulin+high-fat diet for 16 weeks. The total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) in the three groups were compared. The gross aorta and aortic sinus of mice were stained with oil red O, and the area of atherosclerotic plaque was observed and compared. The diversity and structure of the mouse fecal flora were detected by sequencing the V3-V4 region of the 16S rRNA gene, and the levels of metabolites in mouse feces were assessed by gas chromatography-mass spectrometry. The plasma lipopolysaccharide (LPS) levels and aortic inflammatory factors were measured by multi-index flow cytometry (CBA).
Results: [4]
ApoE-/- mice fed with the high-fat diet exhibited an increase of approximately 46% in the area of atherosclerotic lesions, and the levels of TC, TG and LDL-C were significantly increased (P < 0.05) compared with levels in the normal diet group. After inulin was added to the high-fat group, the area of atherosclerotic lesions, the level of serum LPS and aortic inflammation were reduced, and the levels of TC, TG and LDL-C were decreased (P < 0.05). Based on 16S rRNA gene detection, we found that the composition of the intestinal microbiota, such as Prevotella, and metabolites, such as L-arginine, changed significantly due to hyperlipidemia, and the dietary inulin intervention partially reversed the relevant changes.
Conclusion: [4]
Inulin can inhibit the formation of atherosclerotic plaques, which may be related to the changes in lipid metabolism, the composition of the intestinal microbial community and its metabolites, and the inhibition of the expression of related inflammatory factors. Our study identified the relationships among the characteristic intestinal microbiota, metabolites and atherosclerosis, aiming to provide a new direction for future research to delay or treat atherosclerosis by changing the composition and function of the host intestinal microbiota and metabolites.

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Rat high-cholesterol diet model: Male Sprague-Dawley rats were randomly divided into control diet group and high-cholesterol diet group (1% cholesterol + 10% lard) with or without 5% (w/w) Inulin supplementation. Rats were fed for 8 weeks, with food intake and body weight monitored weekly. At the end of the experiment, serum was collected to measure lipid profiles (TC, LDL-C, HDL-C, TG) [1]
- Mouse colon carcinogenesis model: Female C57BL/6 mice were intraperitoneally injected with AOM (10 mg/kg) once weekly for 3 weeks to induce colon tumors. From the first AOM injection, mice were fed a diet containing 10% (w/w) Inulin for 24 weeks. At sacrifice, colon tissues were collected to count tumors and analyze histopathology [3]
- ApoE-/- mouse atherosclerosis model: 6-week-old ApoE-/- mice were fed a Western diet (21% fat + 0.15% cholesterol) with or without 8% (w/w) Inulin for 12 weeks. Aortic tissues were collected for plaque area measurement (Oil Red O staining), and serum was analyzed for cytokines and SCFAs [4]
- Obese mouse metabolic disorder model: Male C57BL/6 mice were fed a high-fat diet (45% fat) for 8 weeks to induce obesity, then supplemented with 6% (w/w) Inulin for another 10 weeks. OGTT was performed to assess glucose tolerance, and gut microbiota composition was analyzed by 16S rRNA sequencing [5]

Poorly absorbed in the small intestine: Inulin is not hydrolyzed by human digestive enzymes (amylase, lactase) and reaches the colon intact [1, 2]
- Metabolized by colonic microbiota: Fermented into SCFAs (acetate, propionate, butyrate) in the colon, with ~95% of SCFAs absorbed into the bloodstream [2, 5]
- No significant systemic distribution: Unfermented Inulin is excreted in feces, accounting for ~5-10% of the administered dose [1]
- SCFAs derived from Inulin have a plasma half-life of ~1.5 hours, primarily metabolized in the liver and peripheral tissues [5]

Acute toxicity: LD50 > 20 g/kg (oral in rats); no mortality or acute adverse effects at doses up to 20 g/kg [1]
- Subchronic toxicity: Daily dietary supplementation of 10% (w/w) Inulin for 6 months in rats caused no significant changes in body weight, liver/kidney function (ALT, AST, creatinine), or hematological parameters [1, 3]
- Gastrointestinal tolerance: Mild and transient bloating, flatulence, or diarrhea reported in humans at doses > 20 g/day; no adverse effects at doses ≤15 g/day [4, 5]
- No genotoxicity or carcinogenicity: Negative in Ames test and animal carcinogenesis models [3]

[1]. J Nutr.1998 Jan;128(1):11-9;
[2]. J Appl Bacteriol.1993 Oct;75(4):373-80;
[3]. Carcinogenesis.1998 Feb;19(2):281-5.
[4]. Coron Artery Dis. 2024 May 17. doi: 10.1097/MCA.0000000000001377.
[5]. Int J Mol Sci. 2024 May 16;25(10):5418. doi: 10.3390/ijms25105418.

Inulin is a naturally occurring fructan polysaccharide found in plants (e.g., chicory, garlic, onions), classified as a soluble dietary fiber and prebiotic [1, 2, 5]
- Core mechanism of action: Acts as a prebiotic to selectively stimulate the growth and activity of beneficial gut bacteria (Bifidobacterium, Lactobacillus), leading to increased SCFA production. SCFAs regulate gut homeostasis, lipid metabolism, inflammation, and cell proliferation [2, 4, 5]
- Potential therapeutic applications: Metabolic disorders (dyslipidemia, type 2 diabetes, obesity), colorectal cancer prevention, and atherosclerosis management [1, 3, 4, 5]
- Clinically recognized as safe (GRAS) by regulatory authorities, with wide use in food and dietary supplements [1, 5]
- Differentiates from other fibers by its specific fermentation profile, preferentially promoting beneficial microbiota without stimulating pathogenic bacteria growth [2]

C6NH10N+2O5N+1

490.411

285.101

9005-80-5

254762074

White to off-white solid powder

1,35 g/cm3

563.5±60.0 °C at 760 mmHg

176-181ºC

294.6±32.9 °C

0.0±1.5 mmHg at 25°C

1.665

Plant/Helianthus tuberosus

1.91

78.29

C1(O)[C@](CO)(OC[C@]2(O[C@H]3OC(CO)[C@@H](O)C(O)C3O)C(O)C(O)[C@@H](CO)O2)O[C@H](CO)C1O

UMGSZTYVVMHARA-RYKCJHNISA-N

InChI=1S/C17H30O16/c18-1-5-7(21)12(26)16(3-20,31-5)29-4-17(13(27)8(22)6(2-19)32-17)33-15-11(25)9(23)10(24)14(28)30-15/h5-15,18-28H,1-4H2/t5-,6-,7-,8-,9+,10+,11-,12+,13+,14+,15-,16-,17+/m1/s1

(2S,3S,4S,5R,6R)-6-(((2S,3S,4S,5R)-2-((((2R,3S,4S,5R)-3,4-dihydroxy-2,5-bis(hydroxymethyl)tetrahydrofuran-2-yl)oxy)methyl)-3,4-dihydroxy-5-(hydroxymethyl)tetrahydrofuran-2-yl)oxy)tetrahydro-2H-pyran-2,3,4,5-tetraol

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)

配方 1 中的溶解度: ≥ 2.5 mg/mL (Infinity mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (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 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.5 mg/mL (Infinity mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (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 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: Water soluble

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配方 4 中的溶解度: 27.5 mg/mL (Infinity mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶.

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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。