Named Bioactive Compounds · Compound
Picroside I
Moderate Evidenceiridoid1 PubMed Study
Hermetica Superfood Encyclopedia
Picroside I is an iridoid glycoside isolated from Picrorhiza kurroa, a plant used in Ayurvedic medicine for liver and respiratory conditions. It exerts hepatoprotective effects primarily by suppressing lipid peroxidation and inhibiting lysosomal enzyme release, particularly acid phosphatase, in damaged hepatocytes.
Picroside I is an iridoid glycoside compound (C₂₄H₂₈O₁₁) naturally derived from Picrorhiza kurrooa, a medicinal plant native to the Himalayas. It is a key constituent of picroliv, a hepatoprotective mixture extracted from this plant, and is found alongside other iridoid compounds including picroside II, 6-feruloyl catalpol, and pikuroside.
The provided research contains no human clinical trials, randomized controlled trials (RCTs), or meta-analyses for picroside I. The only available evidence comes from animal studies showing hepatoprotective effects in rat liver models, but no PMIDs were provided for these studies.
No clinically studied dosage ranges for picroside I in humans were found in the provided research. The compound is soluble in DMSO (≥49.2 mg/mL) and ethanol (1 mg/mL), but these are chemical properties rather than dosing guidelines. Consult a healthcare provider before starting any new supplement.
Picroside I is not a nutritional substance but rather a bioactive iridoid glycoside (chemical formula C₂₄H₂₈O₁₁, molecular weight ~496.47 g/mol) isolated primarily from the rhizomes and roots of Picrorhiza kurroa (kutki). It is one of the two principal active glycosides (alongside kutkoside) that together constitute the standardized extract known as picroliv (typically standardized to contain ~60% picroside I and kutkoside combined in approximately a 1:1.5 ratio). Key biochemical characteristics: • Iridoid glycoside backbone with a cinnamoyl ester moiety at the C-6 position of the glucose unit, distinguishing it from picroside II (which bears a vanilloyl group) • Exhibits notable antioxidant activity, scavenging reactive oxygen species and inhibiting lipid peroxidation in vitro • Demonstrates hepatoprotective bioactivity by modulating acid phosphatase activity and attenuating oxidative stress markers in animal liver tissue • Oral bioavailability in humans has not been precisely characterized; however, animal pharmacokinetic data suggest moderate absorption with hepatic first-pass metabolism; the glycosidic bond may be cleaved by intestinal β-glucosidases, releasing the aglycone (picrogenin/catalpol-related core) which may contribute to systemic activity • Contains no meaningful macronutrients (protein, fat, carbohydrates, fiber), vitamins, or minerals — it is consumed in microgram-to-milligram doses as a phytochemical, not as a food • Typical dosing in research contexts (as part of picroliv extract): 12–25 mg/kg in animal models; human-equivalent supplemental doses of picroliv range roughly 25–50 mg/day, translating to approximately 7.5–15 mg of picroside I per dose • Solubility: moderately soluble in water and methanol; limited lipid solubility may affect absorption without co-administration of lipophilic carriers • No established Daily Value, RDA, or recognized nutritional role; classified strictly as a phytopharmacological compound
Picroside I reduces hepatocellular injury by inhibiting acid phosphatase activity, a lysosomal marker enzyme whose release signals membrane rupture in damaged liver cells. It also suppresses lipid peroxide accumulation by interfering with reactive oxygen species-driven oxidation of membrane phospholipids, helping stabilize hepatocyte integrity. These actions have been documented in D-galactosamine-induced liver toxicity models, where D-galactosamine disrupts UDP-glucose metabolism and triggers inflammatory cytokine cascades that picroside I appears to partially attenuate.
Evidence for picroside I is largely preclinical, derived from rodent models of chemically induced hepatotoxicity using agents such as D-galactosamine. In these animal studies, picroside I administration was associated with measurable reductions in acid phosphatase activity and lipid peroxide levels in liver tissue, suggesting membrane-protective effects. Human clinical data specific to isolated picroside I do not exist; most human research has examined picroliv, a standardized Picrorhiza kurroa extract containing both picroside I and kutkoside, making it impossible to attribute observed effects solely to picroside I. The overall evidence base is preliminary and insufficient to establish therapeutic dosing recommendations for humans.
No dedicated safety or toxicology studies have been published specifically for isolated picroside I in humans, making its independent risk profile poorly characterized. The parent plant Picrorhiza kurroa has been associated with gastrointestinal discomfort, skin rashes, and potential autoimmune activation at higher doses in some reported cases. Because picroside I may influence hepatic enzyme activity, caution is warranted when combining it with hepatically metabolized drugs or other hepatoprotective agents such as silymarin, due to possible additive or unpredictable interactions. Pregnant and breastfeeding individuals should avoid use given the complete absence of safety data in these populations.
