Traditionally used for
- Cough & breathing
- Digestion
- Urinary & fluids
- Skin
- Liver & jaundice
Cautions & contraindications
- Pregnancy
- Liver conditions
- Toxic — professional use only
☯ TCM Properties
Controls pain; Stops cough; Promotes diuresis; Reduces toxicity
Traditional Chinese Uses
Bai Qu Cai is the aerial part of Chelidonium majus (greater celandine), a poppy-family herb with orange latex. Bitter and pungent with a toxic designation (Pharmacopoeia: bitter, cool), entering the Lung, Heart and Kidney (or Lung and Stomach) channels, it alleviates pain, stops cough, promotes urination and resolves toxicity. It is used for gastrointestinal and epigastric pain, chronic and whooping cough, edema and jaundice, and topically for sores, swellings and snake or insect bites.
The plant is rich in benzophenanthridine alkaloids and is officially classed as toxic; clinically significant hepatotoxicity has been documented with internal use. It is therefore given only in small, carefully controlled doses (roughly 3–6 g decocted) and avoided in liver-compromised patients.
Western Herbalism Properties
Relationships
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Botanical Description
Bai Qu Cai corresponds to Chelidonium majus, the greater celandine, a perennial herb of the poppy family Papaveraceae growing 30 to 80 centimetres tall. All parts of the plant exude a thick, bright orange-yellow latex when broken, which is a defining diagnostic character. Stems are erect, slender, and sparsely branched, bearing alternate, pinnately divided leaves whose lobes are themselves rounded and shallowly toothed, glaucous beneath. From late spring through summer the plant produces loose terminal umbels of four-petalled bright yellow flowers about 2 centimetres across, followed by slender, cylindrical capsules 3 to 5 centimetres long that split lengthwise to release shiny black seeds bearing white elaiosomes. The species is native to Europe and western Asia and is widely naturalised in China, North America, and elsewhere, favouring shaded, disturbed ground.
Active Constituents
Chelidonine
Benzophenanthridine isoquinoline alkaloidConcentration: one of the principal benzophenanthridines of the herb; total alkaloid content of the plant is reported at roughly 0.27-2.25% in the aerial parts and 3-4% in the root, with the latex far richer than either
Chelidonine is an antispasmodic and mitotic-spindle-active alkaloid and is the constituent most often held responsible for the herb's traditional antispasmodic and analgesic effect on the stomach and gallbladder. It is also implicated in the herb's liver toxicity: hepatic demethylation yields phenolic metabolites that oxidise to quinones, which conjugate glutathione and deplete hepatic glutathione stores.
Chelerythrine
Benzophenanthridine isoquinoline alkaloidA quaternary benzophenanthridine alkaloid and a well-characterised protein kinase C inhibitor. It is directly cytotoxic to hepatocytes in vitro and, with sanguinarine, contributes to the herb's cytotoxic and pro-apoptotic profile rather than to any therapeutic effect at ordinary doses.
Sanguinarine
Benzophenanthridine isoquinoline alkaloidConcentration: concentrated in the root rather than the aerial parts
The most cytotoxic of the common Chelidonium alkaloids. It inhibits Na+/K+-ATPase, induces chromosome breaks and DNA damage, and is a potent inhibitor of interleukin-1 beta secretion in stimulated human neutrophils. Its genotoxicity is a substantive safety concern for prolonged internal use.
Coptisine
Protoberberine isoquinoline alkaloidConcentration: the dominant protoberberine of the aerial parts and of in vitro shoot cultures
Coptisine carries much of the choleretic and antimicrobial activity attributed to greater celandine, and suppresses TNF-alpha release from stimulated neutrophils.
Berberine
Protoberberine isoquinoline alkaloidPresent as a minor protoberberine. Berberine is a documented inhibitor of CYP3A4 and CYP2D6 and a P-glycoprotein substrate, so its presence is the main theoretical basis for pharmacokinetic interactions with this herb.
Protopine
Protopine-type isoquinoline alkaloidA smooth-muscle relaxant alkaloid that contributes to the antispasmodic action on the biliary tract and gastrointestinal wall.
⚠ Drug Interactions
Hepatotoxic drugs (paracetamol/acetaminophen, methotrexate, isoniazid, azole antifungals, amiodarone)
Greater celandine is an established cause of herb-induced liver injury. In a German spontaneous-report series of 22 cases assessed by RUCAM, causality was probable in a substantial subset; the pattern is idiosyncratic hepatocellular injury resembling acute viral hepatitis, with latency of about three weeks to four and a half months. Mechanistically, chelidonine metabolites deplete hepatic glutathione and the benzophenanthridine alkaloids are directly cytotoxic to rat hepatocytes in vitro. Adding a second hepatotoxin removes the reserve that would otherwise absorb this injury. Recurrence on rechallenge has been documented, so re-exposure is contraindicated.
Clinical note: Do not prescribe internally alongside any drug with known hepatotoxic potential. If the herb is used at all, check ALT/AST and bilirubin at baseline and again at 4 and 8 weeks, stop immediately on any rise or on nausea, dark urine or jaundice, and never rechallenge a patient who has reacted before.
Alcohol and other chronic hepatic stressors
The injury mechanism is glutathione-depleting and idiosyncratic. Regular alcohol intake lowers hepatic glutathione and is a recognised co-factor in drug- and herb-induced liver injury generally, though the published Chelidonium case series do not isolate alcohol as an independent risk factor.
Clinical note: Avoid internal use in anyone with regular alcohol intake, pre-existing liver disease, or abnormal baseline liver enzymes.
Proprietary preparations containing Chelidonium majus (e.g. STW 5 / Iberogast)
Chelidonium is a component of widely sold over-the-counter digestive preparations, and acute liver injury has been reported in a patient taking such a product. A patient may therefore already be taking greater celandine without describing it as a herb, so the exposure adds to any prescribed decoction.
Clinical note: Ask specifically about over-the-counter digestive and gallbladder preparations before prescribing, and count them as part of the total Chelidonium dose.
QT-prolonging drugs (e.g. sotalol, amiodarone, macrolides, some antipsychotics)
Several Chelidonium alkaloids block hERG potassium channels and delay cardiac repolarisation in preclinical work. No human case of QT prolongation attributable to greater celandine has been published, so this remains an extrapolation from in vitro channel data rather than a documented clinical event.
Clinical note: Treat as a reason for caution rather than an established interaction; avoid internal use in patients with known long QT syndrome or on multiple QT-prolonging agents.
CYP3A4 and CYP2D6 substrates with a narrow therapeutic index (e.g. ciclosporin, tacrolimus, metoprolol)
Chelidonium contains berberine and coptisine, and berberine is a documented inhibitor of CYP3A4 and CYP2D6. However, no pharmacokinetic study of whole Chelidonium majus extract against a CYP probe cocktail has been published, and the berberine content of the herb is minor, so this is an inference from constituent chemistry and not a measured interaction.
Clinical note: Flag rather than assume. If the herb is unavoidable in a patient on a narrow-index CYP3A4 or CYP2D6 substrate, monitor drug levels or clinical effect.
Dosage
| Form | Amount | Frequency | Duration | Population | Notes |
|---|---|---|---|---|---|
| decoction | 9–18 g | — | — | — | ChP 2025.. Corrected from a generic 6-15g decoction filler value generated from tcm_category. |
Evidence Tier
Limited evidence · 1 studyRecorded studies by study design, strongest design at the top. This is a study-design tier only, not a GRADE rating: it does not weigh risk of bias, consistency or precision.
Systematic review / meta-analysis
0
Randomized controlled trial
0
Other clinical trial
0
Observational / case report
0
In vitro / animal
1
1 verified · 0 unverified
Other / unclassified
0
Verified: design read from PubMed for a DOI that resolves to the cited paper Unverified: taken from the study's recorded description
Clinical Studies
Characterization of the cytotoxicity of selected Chelidonium alkaloids in rat hepatocytes
Compared the cytotoxic potency of individual Chelidonium majus alkaloids in rat hepatocytes, establishing that the benzophenanthridine alkaloids are directly toxic to liver cells and providing an in vitro correlate for the clinical hepatotoxicity reported with the herb.
⚠ Safety & Contraindications
- Pregnancy
- Liver conditions
- Toxic — professional use only
Contraindications
Contraindicated in pregnancy and in any pre-existing liver disease.
Safety Warnings
- Hepatotoxicity is idiosyncratic rather than dose-dependent — it can occur at ordinary doses.
- Liver function should be monitored; stop at once if jaundice, dark urine or right-sided abdominal pain appear.
- Not to be combined with other hepatotoxic drugs.
Regulatory Status
- Restricted in several European countries following reports of hepatotoxicity; internal use of Chelidonium is limited or prohibited in some jurisdictions.
⚠ Toxicity Information
Nausea and abdominal pain; the significant risk is idiosyncratic hepatotoxicity, with cholestatic hepatitis well documented in the European literature and cases of acute liver failure reported.
Historical Texts
Jiu Huang Ben Cao (Materia Medica for Famine Relief)
Ming dynasty, 1406De Materia Medica (Dioscorides)
Greco-Roman, 1st century CEChinese Pharmacopoeia (Zhonghua Renmin Gongheguo Yaodian)
Modern, 2020 editionReferences
- Li XL, Sun YP, Wang M, Wang ZB, Kuang HX. Alkaloids in Chelidonium majus L: a review of its phytochemistry, pharmacology and toxicology . Frontiers in Pharmacology (2024) [DOI]
- Teschke R, Glass X, Schulze J. Herbal hepatotoxicity by Greater Celandine (Chelidonium majus): Causality assessment of 22 spontaneous reports . Regulatory Toxicology and Pharmacology (2011) [DOI]
- Maggini V, Lombardi N, Crescioli G, Gallo E, Sivelli F, Gensini GF, Vannacci A, Firenzuoli F. Chelidonium majus: Relevant safety aspects of a hepatotoxic plant, trawling the web . Phytotherapy Research (2019) [DOI]
- Zielinska S, Jezierska-Domaradzka A, Wojciak-Kosior M, Sowa I, Junka A, Matkowski AM. Greater Celandine's Ups and Downs−21 Centuries of Medicinal Uses of Chelidonium majus From the Viewpoint of Today's Pharmacology . Frontiers in Pharmacology (2018) [DOI]
- Power S, Barritt AS. A Yellow Flower With Jaundice Power: Liver Injury Attributed to Greater Celandine . ACG Case Reports Journal (2024) [DOI]
- Leroy A, Perrin H, Porret R, Sempoux C, Chtioui H, Fraga M, Bart PA. Iberogast®-Induced Acute Liver Injury—A Case Report . Gastro Hep Advances (2022) [DOI]
- Romanu R, Liga S, Tripon MR, Huiban F, Iliescu D, Dehelean CA, Tulcan C. Chelidonium majus L.: A Current Perspective on Isoquinoline Alkaloids, Emerging Phytochemicals, Alkaloid Biosynthesis, and Biological Activities . Plants (2025) [DOI]
- National Institute of Diabetes and Digestive and Kidney Diseases. GREATER CELANDINE . A Field Guide to Urban Plants (2025) [DOI]
This information is for educational purposes only and is not intended to replace professional medical advice. Always consult a qualified healthcare provider before using any herbal remedy, especially if you are pregnant, nursing, or taking medications.
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