Qing Mu Xiang
StarAristolochia debilis Siebold & Zucc.
Traditionally used for
- Digestion
- Urinary & fluids
- Skin
Cautions & contraindications
- Kidney conditions
- Toxic — professional use only
☯ TCM Properties
Promotes the flow of Qi, alleviates pain, resolves edema, clears Heat and removes toxicity
Traditional Chinese Uses
Qing Mu Xiang is the root of Aristolochia debilis. Traditional texts, in which it is pungent, bitter and cold entering the Liver and Stomach channels, used it to promote Qi movement and relieve epigastric and abdominal pain, clear Heat and resolve toxicity, and reduce swelling, including topical use for sores, abscesses and snakebite.
Critical safety warning: like all Aristolochia species, it contains aristolochic acid, which is nephrotoxic and carcinogenic and has caused aristolochic acid nephropathy and urothelial cancers. For this reason it has been removed from the Chinese Pharmacopoeia and banned or withdrawn in many countries. It is no longer recommended for any internal or medicinal use, and this entry is provided as historical information only, not as an endorsement.
Pharmacological Effects
- Hypotensive: Decoction and extracts lowered blood pressure in several animal species (i.v. fast, i.m. slower, oral slowest), including hypertensive dogs and rats; not blocked by vagotomy or atropine. Magnoflorine identified as a hypotensive principle (2 mg/kg i.v. in cats), acting as a ganglion blocker.
- Antibacterial and immuno-incremental: Total alkaloids inhibited S. aureus, P. aeruginosa, E. coli and Proteus in vitro; aristolochic acid A (50 µg/kg i.p.) protected mice against bacterial infection and stimulated macrophage phagocytosis and other immune parameters in mice and guinea pigs.
- Antineoplastic: Aristolochic acid A inhibited sarcoma-37 cells in vitro, prolonged survival of mice with ascitic sarcoma-37 (1.25–5 mg/kg i.p. x5), inhibited solid sarcoma-37 and methylcholanthrene tumors; sex-dependent activity in Ehrlich ascites.
- Other effects: Aristolochic acid A increased cellular oxygen consumption and leukocyte metabolic activity; showed anti-implantation/early pregnancy-interrupting (contraceptive) effects in female mice and terminated pregnancy after intra-amniotic injection in dogs and rats.
Source: Zhu YP. Chinese Materia Medica: Chemistry, Pharmacology and Applications. Harwood Academic, 1998, p. 380.
Relationships
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Botanical Description
Qing Mu Xiang in current Chinese pharmacopoeia tradition denotes the dried root of Aristolochia debilis Sieb. & Zucc. (Aristolochiaceae), a slender perennial twiner of central and southern China with cordate-hastate leaves and small S-curved trumpet-shaped purple-veined flowers, also the source of the fruit drug Ma Dou Ling. WARNING: All Aristolochia species contain aristolochic acids, potent nephrotoxins and IARC Group 1 human carcinogens implicated in aristolochic acid nephropathy and urothelial carcinoma; these herbs are banned or restricted in the United States, European Union, and many other jurisdictions and were removed from the 2005 and later Chinese Pharmacopoeia. Historically classified as acrid, bitter, cold, and slightly toxic in TCM, it moved qi, relieved pain, and clear heat for epigastric pain, dysentery, and snakebite. Note: in some older materia medica the name Qing Mu Xiang was also applied to Saussurea costus root, distinct from the modern Aristolochia identity.
Active Constituents
Aristolochic acid I (aristolochic acid A)
Nitrophenanthrene carboxylic acidConcentration: 1.19-4.71 mg/g of the dried root (Qing Mu Xiang) and 0.69-1.77 mg/g of the dried fruit (Ma Dou Ling) of this same species by HPLC; a separate survey of 11 commercial Aristolochia debilis samples found 0.9-2 mg/g
A proven human carcinogen and nephrotoxin, not a therapeutic constituent. It is classified by IARC in Group 1 (carcinogenic to humans). It enters proximal tubular cells through the organic anion transporters OAT1 and OAT3, is reduced to an aristolactam-nitrenium ion, and forms 7-(deoxyadenosin-N6-yl)-aristolactam DNA adducts that resist nucleotide excision repair and persist in renal tissue for years. Those adducts generate a distinctive A:T to T:A transversion signature in TP53 exons 5-8. The resulting injury is interstitial fibrosis with tubular atrophy progressing to end-stage renal disease, and upper urinary tract urothelial carcinoma. No threshold below which this does not occur has been demonstrated, and the damage is irreversible.
Aristolochic acid II
Nitrophenanthrene carboxylic acidConcentration: 0.24-1.69 mg/g of the dried root (Qing Mu Xiang) and 0.02-0.18 mg/g of the dried fruit (Ma Dou Ling)
The second major aristolochic acid. It is bioactivated by the same nitroreduction pathway to a dA-aristolactam II adduct. Co-exposure to aristolochic acids I and II has been shown in rats to increase the DNA adduct burden responsible for aristolochic acid I carcinogenicity, so its presence adds to rather than dilutes the hazard.
Aristolochic acid IVa
Nitrophenanthrene carboxylic acid analogueConcentration: 0.76-3.36 mg/g of the dried fruit (Ma Dou Ling); not detected in the root in the same survey
An aristolochic acid analogue quantified as a major component of the fruit. Analogues of this family are used together as markers of aristolochic acid exposure in herbal material; they are not separable from the toxic fraction.
Aristolactam I (aristololactam I)
Phenanthrene lactam alkaloidConcentration: 0.07-0.36 mg/g of the dried fruit (Ma Dou Ling); not detected in the root in the same survey
The reduced lactam corresponding to aristolochic acid I, present in the plant and also formed in the body during bioactivation. Aristolactams and their derivatives, not only the parent acids, have been implicated in the aristolochic acid mutational signature found in liver cancers across Asia.
Magnoflorine
Quaternary aporphine alkaloidAn alkaloid reported in the dried fruits and roots of Aristolochia debilis alongside cyclanoline. It is not the toxicologically relevant constituent, and its presence is of no clinical significance next to the aristolochic acid content.
⚠ Drug Interactions
Aucklandia lappa root (Mu Xiang), where Qing Mu Xiang is the documented substitute
Radix Aristolochiae (Qing Mu Xiang), from Aristolochia debilis and Aristolochia contorta, is documented as being used confusedly as a substitute for Radix Aucklandiae (Mu Xiang, Aucklandia lappa) because of similar morphology and near-identical trade names. Molecular authentication and cytotoxicity work on herbal materials confused with Aristolochia herbs confirms this substitution occurs in commerce. The practical consequence is that a prescription for Mu Xiang can be filled with aristolochic acid-containing material without the practitioner or patient knowing.
Clinical note: Mu Xiang (Aucklandia lappa) and Qing Mu Xiang (Aristolochia debilis) are different plants in different families; the shared name is the hazard. Source Aucklandiae Radix only from suppliers who authenticate species and test for aristolochic acids, and never accept 'qing mu xiang' as a synonym or substitute for it.
Akebia stem (Mu Tong) and Stephania tetrandra root (Fang Ji), the other Aristolochia substitution pairs
Aristolochia manshuriensis (Guan Mu Tong) has been supplied for Akebia (Mu Tong), and Aristolochia fangchi (Guang Fang Ji) for Stephania tetrandra (Han Fang Ji). The latter substitution in a Belgian weight-loss regimen from 1992 produced rapidly progressive interstitial nephropathy and urothelial carcinoma in exposed women, with aristolactam-DNA adducts demonstrated in the excised tissue. A Taiwanese population-based case-control study found a dose-dependent increase in urinary tract cancer risk with prescribed aristolochic acid-containing herbs. Aristolochia debilis sits in the same substitution family and its root and fruit carry comparable or higher aristolochic acid loads than Guan Mu Tong's fruit.
Clinical note: Treat any Mu Tong, Fang Ji, Mu Xiang or Xi Xin of unverified origin as potentially aristolochic acid-containing and require species authentication plus analytical testing. A patient with unexplained interstitial nephropathy or upper tract urothelial cancer should be asked specifically about herbal use, including years earlier, because the adducts and the risk persist.
Nephrotoxic drugs (NSAIDs, aminoglycosides, cisplatin, calcineurin inhibitors, iodinated contrast)
Aristolochic acid injures the proximal tubule selectively after OAT-mediated uptake, producing extensive interstitial fibrosis with tubular atrophy. Any co-administered agent that damages the same segment adds to that injury, and reduced renal perfusion from NSAIDs or volume depletion prolongs tubular exposure. This is mechanistic and pharmacological reasoning rather than a formal interaction study, because the exposure itself is not one that can ethically be studied.
Clinical note: There is no combination and no monitoring schedule that makes this exposure acceptable. The action is to stop the aristolochic acid source, not to manage the co-medication around it.
Organic anion transporter substrates and inhibitors (probenecid, methotrexate, cidofovir)
Aristolochic acid accumulates in proximal tubular cells via OAT1 and OAT3, which is why the toxicity is renal and segment-specific. Substrates and inhibitors of those transporters therefore compete with it. This is recorded here because the transporter biology is established, not because any co-medication offers protection: no drug has been shown to prevent aristolactam-DNA adduct formation in exposed people, and adducts already formed persist for years.
Clinical note: Do not read this as a way to give the herb safely. Nothing co-prescribed makes aristolochic acid exposure acceptable, and the carcinogenic risk is not dose-thresholded.
Dosage
| Form | Amount | Frequency | Duration | Population | Notes |
|---|---|---|---|---|---|
| not recommended | Not established — should not be dispensed | — | — | — | **This drug should not be dispensed.** Qing Mu Xiang (青木香) is the root of Aristolochia debilis. All Aristolochia species contain aristolochic acid, which causes irreversible aristolochic acid nephropathy and urothelial carcinoma, and is an IARC Group 1 human carcinogen. Same plant as Ma Dou Ling (which is the fruit); both were delisted. It has no monograph in the Chinese Pharmacopoeia 2020 — the aristolochic-acid drugs were delisted — so no dose is given here and none is defensible. Safe substitutes that ARE in ChP 2020: Mu Tong (Akebiae Caulis, 3–6 g) replaces the Aristolochia 'mu tong' drugs, and Fang Ji (Stephaniae Tetrandrae Radix, 5–10 g) replaces the Aristolochia 'fang ji' drugs. |
Evidence Tier
Moderate evidence · 7 studiesRecorded 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
7
0 verified · 7 unverified
Show 7 studies
- Aristolochic acid-associated urothelial cancer in Taiwan
- Population-Based Case-Control Study of Chinese Herbal Products Containing Aristolochic Acid and Urinary Tract Cancer Risk
- Mutational Signature of Aristolochic Acid Exposure as Revealed by Whole-Exome Sequencing
- Genome-Wide Mutational Signatures of Aristolochic Acid and Its Application as a Screening Tool
- Aristolochic acids and their derivatives are widely implicated in liver cancers in Taiwan and throughout Asia
- Aristolochic acid and the etiology of endemic (Balkan) nephropathy
- Urothelial Carcinoma Associated with the Use of a Chinese Herb (Aristolochia fangchi)
In vitro / animal
0
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
Aristolochic acid-associated urothelial cancer in Taiwan
In Taiwanese patients with upper urinary tract urothelial carcinoma, aristolactam-DNA adducts were detected in renal tissue as a specific biomarker of aristolochic acid exposure, and the tumours carried the characteristic A:T to T:A transversion signature in TP53. The study links Aristolochia-containing herbal use in a population to a molecularly identifiable cancer, establishing causation rather than association.
Population-Based Case-Control Study of Chinese Herbal Products Containing Aristolochic Acid and Urinary Tract Cancer Risk
Population-based case-control study using Taiwan's national prescription database. Prescribed Chinese herbal products containing aristolochic acid were associated with an increased risk of urinary tract cancer, and the risk rose with cumulative estimated aristolochic acid dose. This is the epidemiological counterpart to the molecular evidence, in a population exposed through routine prescribing rather than through a single contaminated product.
Mutational Signature of Aristolochic Acid Exposure as Revealed by Whole-Exome Sequencing
Whole-exome sequencing of upper tract urothelial carcinomas from aristolochic acid-exposed patients revealed an exceptionally high mutation burden dominated by A:T to T:A transversions concentrated on the non-transcribed strand. The signature is distinct from that of tobacco or ultraviolet exposure, making prior aristolochic acid exposure identifiable in an individual tumour years after the herb was taken.
Genome-Wide Mutational Signatures of Aristolochic Acid and Its Application as a Screening Tool
Genome-wide sequencing of aristolochic acid-associated urothelial tumours defined the mutational signature at whole-genome scale and demonstrated it could be used as a screening tool to detect past aristolochic acid exposure in tumours where no exposure history was known. Independent confirmation of the Hoang finding in a separate cohort.
Aristolochic acids and their derivatives are widely implicated in liver cancers in Taiwan and throughout Asia
Sequencing of hepatocellular carcinomas found the aristolochic acid mutational signature in 78% of Taiwanese cases and in a substantial fraction of tumours from elsewhere in Asia, extending the documented harm beyond the kidney and urinary tract to the liver. This is the study that showed the exposure is not a historical curiosity confined to a few outbreaks.
Aristolochic acid and the etiology of endemic (Balkan) nephropathy
Demonstrated that endemic Balkan nephropathy, long of unknown cause, is aristolochic acid nephropathy arising from dietary contamination of wheat with Aristolochia clematitis seed. Aristolactam-DNA adducts were found in renal cortex and the A:T to T:A TP53 signature in the associated urothelial tumours, establishing that chronic low-level dietary exposure is sufficient to cause the disease.
Urothelial Carcinoma Associated with the Use of a Chinese Herb (Aristolochia fangchi)
Of 39 patients with end-stage aristolochic acid nephropathy from a Belgian weight-loss regimen in which Stephania tetrandra had been replaced by Aristolochia fangchi, 18 had urothelial carcinoma on prophylactic nephroureterectomy and 19 more had mild to moderate dysplasia; aristolochic acid-DNA adducts were detected in the tissue. The species here is Aristolochia fangchi, not Aristolochia debilis, but it is the index clinical series for the whole genus and the reason the substitution hazard is taken seriously.
⚠ Safety & Contraindications
- Kidney conditions
- Toxic — professional use only
Contraindications
Its use is cautious in patients with deficiency-cold syndrome. It is not suitable for overdose, which may cause the gastrointestinal reaction, such as nausea and vomiting.
Source: Xi S, Gong Y. Essentials of Chinese Materia Medica and Medical Formulas. Academic Press/Elsevier, 2017, pp. 171–182.
Side Effects
- Aristolochic acid A showed sex-dependent toxicity: acute toxicity higher in males, chronic toxicity affected females more.
Source: Zhu YP. Chinese Materia Medica: Chemistry, Pharmacology and Applications. Harwood Academic, 1998, p. 380.
Safety Warnings
- Aristolochic acid — nephrotoxic and carcinogenic (aristolochic-acid nephropathy, urothelial cancer). Not for internal use; illegal to dispense.
Regulatory Status
- Banned in China (removed from the Pharmacopoeia in 2004); prohibited or restricted in the US/EU. Contains aristolochic acid.
⚠ Toxicity Information
Historical Texts
Kai Bao Ben Cao
Song dynastyBen Cao Gang Mu
Ming dynastyReferences
- Han J, Xian Z, Zhang Y, Liu J, Liang A. Systematic Overview of Aristolochic Acids: Nephrotoxicity, Carcinogenicity, and Underlying Mechanisms . Frontiers in Pharmacology (2019) [DOI]
- Zhang C, Wang X, Shang M, Yu J, Xu Y, Li Z, Lei L, Li X, Cai S, Namba T. Simultaneous determination of five aristolochic acids and two aristololactams in Aristolochia plants by high-performance liquid chromatography . Biomedical Chromatography (2006) [DOI]
- Zhang SH, Wang Y, Yang J, Zhang DD, Wang YL, Li SH, Pan YN, Zhang HM, Sun Y. Comparative Analysis of Aristolochic Acids in Aristolochia Medicinal Herbs and Evaluation of Their Toxicities . Toxins (2022) [DOI]
- Li M, Au KY, Lam H, Cheng L, But PPH, Shaw PC. Molecular identification and cytotoxicity study of herbal medicinal materials that are confused by Aristolochia herbs . Food Chemistry (2014) [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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