Astragalin

Astragalin is a kaempferol-3-O-glucoside flavonoid glycoside found in persimmon leaves, rose hips, and Astragalus species that exerts anti-inflammatory effects primarily by suppressing NF-κB signaling and inhibiting cyclooxygenase-mediated prostaglandin synthesis. Research spanning in vitro and animal models suggests it also modulates apoptotic pathways in cancer cells, though human clinical trials remain limited.

Origin & History

Astragalin is a naturally occurring flavonoid (kaempferol 3-O-β-D-glucopyranoside) first isolated from Astragalus sinicus, appearing as a yellow compound. It occurs in various edible plants including green tea seeds, mulberry fruits and leaves, persimmon leaves, and Astragalus membranaceus roots. Extraction methods include methanolic extraction from fern fronds, enzymatic hydrolysis of tea seed extract (yielding >96% purity), and chromatographic separation techniques.

Historical & Cultural Context

Astragalin is a bioactive constituent in traditional medicinal plants used in Chinese medicine, including Cuscuta chinensis, Astragalus membranaceus, and Morus alba. While these plants have long traditional use for immune support, isolation and bioactivity studies of astragalin itself are modern developments (post-2010).

Health Benefits

• Anti-inflammatory effects demonstrated in vitro by inhibiting nitric oxide (IC50=363 µg/mL), PGE2 (IC50=134 µg/mL), and IL-6 (IC50=289 µg/mL) in LPS-stimulated macrophages (preliminary evidence)
• Anticancer activity shown in mouse xenograft models with oral doses of 25-75 mg/kg inhibiting HCT116 colon cancer cell growth through apoptosis induction and NF-κB pathway suppression (preliminary evidence)
• Cell cycle arrest capabilities demonstrated in vitro through G0/G1 phase arrest via downregulation of CDK2/4 and Cyclin D1/E (preliminary evidence)
• Anti-metastatic potential shown through downregulation of MMP-2/9 proteins in cancer cell models (preliminary evidence)
• Enzyme modulation including iNOS, COX-2, and various kinases (JNK, MAPK, Akt, ERK) based on in vitro studies (preliminary evidence)

How It Works

Astragalin suppresses the NF-κB signaling pathway, reducing transcription of pro-inflammatory mediators including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and interleukin-6 (IL-6), as demonstrated in LPS-stimulated macrophage models. It also activates intrinsic apoptotic cascades by modulating Bcl-2 family protein ratios, upregulating Bax and cleaved caspase-3 while downregulating anti-apoptotic Bcl-2 expression in colorectal cancer cell lines. Additionally, astragalin inhibits MAPK (ERK1/2 and p38) phosphorylation, further attenuating inflammatory cytokine production.

Scientific Research

No human clinical trials, RCTs, or meta-analyses for astragalin were identified; all evidence is limited to preclinical studies. Key animal research includes BALB/c nude mice studies showing tumor growth inhibition at 25-75 mg/kg oral doses through upregulation of pro-apoptotic factors and downregulation of anti-apoptotic proteins (Yang et al., 2021, PMID not provided). In vitro studies demonstrated anti-inflammatory effects in RAW 264.7 macrophages (PMID: 21567414).

Clinical Summary

Current evidence for astragalin is predominantly preclinical. In vitro studies in LPS-stimulated RAW 264.7 macrophages have quantified inhibition of nitric oxide (IC50=363 µg/mL), PGE2 (IC50=134 µg/mL), and IL-6 (IC50=289 µg/mL), establishing a measurable anti-inflammatory potency profile. Mouse xenograft studies using HCT116 colorectal cancer cells demonstrated meaningful tumor growth inhibition at oral doses of 25–75 mg/kg, with dose-dependent responses. No randomized controlled trials in humans have been published as of the latest literature review, meaning all efficacy claims remain preliminary and should not be extrapolated directly to clinical use.

Nutritional Profile

Astragalin (kaempferol-3-O-glucoside) is a flavonoid glycoside compound with molecular formula C21H20O11 and molecular weight of 448.38 g/mol. It is not a food ingredient with macronutrient or micronutrient composition in the traditional sense, but rather a discrete bioactive phytochemical. As a pure compound, it contains no meaningful protein, fat, or fiber content. Bioactive compound concentration: when isolated, it is evaluated at 100% purity in research settings, though in natural plant sources (e.g., rose hips, persimmon leaves, green tea, Moringa oleifera) concentrations typically range from 0.1–2.5 mg/g dry weight depending on plant matrix and extraction method. Bioavailability is limited by its glycosidic form; intestinal hydrolysis by beta-glucosidases cleaves the glucose moiety to release the aglycone kaempferol, which is more readily absorbed. Oral bioavailability studies in rodents suggest moderate absorption with peak plasma concentrations reached within 1–2 hours post-administration. The compound undergoes phase II metabolism (glucuronidation and sulfation) in the intestinal wall and liver. Molecular LogP is approximately 1.58, indicating moderate lipophilicity. No clinically established dietary reference intake or recommended daily amount exists. Solubility in water is low (~0.1 mg/mL at 25°C), which may further limit bioavailability in vivo without formulation enhancement.

Preparation & Dosage

No clinically studied human dosages available. Preclinical mouse studies used 25-75 mg/kg oral doses (theoretical human equivalent ~2-6 mg/kg, not tested). In vitro anti-inflammatory effects observed at 134-363 µg/mL using >96% pure astragalin prepared via enzymatic hydrolysis. Consult a healthcare provider before starting any new supplement.

Synergy & Pairings

Kaempferol, Quercetin, Green tea polyphenols, Curcumin, Resveratrol

Safety & Interactions

Astragalin has not been evaluated in formal human safety trials, so a comprehensive adverse effect profile is not yet established. Animal studies at doses up to 75 mg/kg oral administration have not reported overt toxicity, but species-to-human dose translation requires caution. Because astragalin inhibits COX-2 and prostaglandin synthesis through pathways similar to NSAIDs, concurrent use with anticoagulants such as warfarin or antiplatelet drugs like aspirin may theoretically potentiate bleeding risk and warrants medical supervision. Pregnant or breastfeeding individuals should avoid supplementation due to a complete absence of safety data in these populations.