Traditionally used for
- Headaches
- Dizziness
- Eye health
- Cough & breathing
- Digestion
- Bowel health
- Skin
Cautions & contraindications
- Young children
- Heart conditions
- Liver conditions
- Toxic — professional use only
☯ TCM Properties
Clears Liver Fire, strengthen the Stomach, clears the Lungs, disperses swelling, removes toxicity, relaxes the bowels and clears vision
Traditional Chinese Uses
Wang Jiang Nan Zi is the seed of Senna occidentalis (coffee senna, Fabaceae). Bitter (and reputedly sweet) with a cold nature, it enters the Stomach and Large Intestine channels to clear Liver Fire and brighten the eyes, strengthen the Stomach, clear the Lungs, disperse swelling and toxicity, and gently loosen the bowels. Traditional indications include red, swollen, painful eyes and headache or dizziness from Liver-fire rising, indigestion and stomach pain, constipation, damp-heat dysentery, and sores and boils.
It is decocted in small amounts (about 6–9 g) or given as a powder, and must be properly processed before use.
Relationships
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Botanical Description
Senna occidentalis, coffee senna, is a robust annual to short-lived perennial subshrub of the Fabaceae family (Caesalpinioideae), native to the American tropics and naturalized throughout warm regions worldwide, including southern China. The plant grows erect to about one to two meters, with smooth green to purplish stems and alternate, even-pinnate compound leaves bearing four to six pairs of ovate-lanceolate leaflets that emit a fetid odor when crushed. Bright yellow five-petalled flowers are borne in short axillary racemes, producing slender flattened curved pods up to twelve centimeters long. The pods contain numerous flat, dull-brown seeds arranged transversely; these seeds, sometimes roasted as a coffee substitute, are the principal medicinal part used in TCM and have a hard, dark seedcoat that requires processing.
Active Constituents
Rhein
AnthraquinoneOne of the anthraquinones characterised in S. occidentalis seed and detected in the biofluids of poisoned children. It has the highest serum albumin binding affinity of the group and the highest cytotoxicity, and it oxidises glutathione to GSSG (30 percent) more than the other anthraquinones tested. It is a central suspect in the hepato-myo-encephalopathy syndrome.
Emodin
AnthraquinoneShows the strongest binding to calf thymus DNA of the seed anthraquinones (Ka = 3.854 x 10^4 L/mol/s), which the authors link to its high cytotoxicity. Present in the seed and detected in the serum of children with hepato-myo-encephalopathy.
Aloe-emodin
AnthraquinoneBinds DNA strongly (Ka = 0.961 x 10^4 L/mol/s), forms a glutathione conjugate, and oxidises glutathione to GSSG by around 28 percent, depleting cellular thiol defences. Together with rhein and emodin it accounts for most of the measured cytotoxicity of the seed anthraquinone fraction.
Chrysophanol
AnthraquinonePresent in the seed but shows very low DNA binding and correspondingly lower cytotoxicity than rhein, emodin or aloe-emodin. Its presence is not reassuring, since it travels with the more toxic congeners.
Physcion
AnthraquinoneIsolated from the roots of this species and also present in the seed. It has low DNA binding but forms a glutathione conjugate. It is one of the five anthraquinones the Indian outbreak investigators quantified in seed and in patient biofluids.
Dianthrone
Anthraquinone-derived dianthroneThe anthraquinone-derived compound identified in S. occidentalis seed as the principle responsible for the characteristic mitochondrial myopathy of livestock poisoning. Affected muscle shows mitochondrial swelling, loss of matrix, fragmented cristae, reduced cytochrome oxidase activity and glycogen depletion. This is a different toxic mechanism from the simple laxative action of anthraquinone glycosides.
C-glycosidic flavonoids
Flavone C-glycosideA group of C-glycosyl flavones characterised from this species. They are not implicated in the toxicity and are of chiefly chemotaxonomic interest, useful for distinguishing S. occidentalis material from related Senna drugs.
⚠ Drug Interactions
Senna obtusifolia (Jue Ming Zi) and Senna alexandrina (Fan Xie Ye) — misidentification or substitution
S. occidentalis shares the Cassia synonymy, the trade descriptor coffee senna, the yellow-flowered habit and the flat pod of its relatives, and the Chinese name Jia Jue Ming (false Jue Ming Zi) records the confusion directly. But the toxicological profiles differ sharply: it is S. occidentalis seed, not Jue Ming Zi, that is tied to the Indian childhood hepato-myo-encephalopathy outbreaks, and neither S. occidentalis nor S. obtusifolia is a safe stand-in for the other, since both are documented livestock myotoxins in Brazil while Fan Xie Ye is a conventional stimulant laxative with none of this profile.
Clinical note: Never accept Jue Ming Zi, Fan Xie Ye or Wang Jiang Nan Zi on pinyin or Cassia name alone. Require the binomial on the certificate of analysis and reject material identified only as Cassia sp. This herb is not interchangeable with either of the other two in any formula.
Grain, pulse, soybean and animal feed contaminated with Senna occidentalis seed
S. occidentalis is a weed of cultivated land and a recognised contaminant of agricultural commodities. Livestock poisoning almost always occurs through feed contaminated with the seed, and the recurrent childhood outbreaks in western Uttar Pradesh and Uttaranchal, seen between September and December and originally misdiagnosed as viral encephalitis, were traced to unintentional ingestion of the seed by malnourished children.
Clinical note: Treat this as a herb where the main clinical hazard is unrecognised rather than prescribed exposure. In a child from an endemic area presenting with fever, vomiting, abnormal behaviour, rising transaminases and a raised creatine phosphokinase, ask specifically about seed ingestion. Do not prescribe this herb to children at all.
Hepatotoxic drugs (paracetamol, methotrexate, isoniazid, rifampicin, azole antifungals, valproate)
Rats fed 0.5 to 2 percent ground seed for 28 days developed significant rises in transaminases, alkaline phosphatase and lactate dehydrogenase with histopathological hepatic lesions; rabbits fed 4 percent seed died in the third week with centrilobular hepatic degeneration. Mechanistically the anthraquinones bind DNA, generate reactive oxygen species and deplete glutathione by oxidising it to GSSG, which removes the same defence that protects against paracetamol and other reactive-metabolite hepatotoxins.
Clinical note: Do not co-prescribe with any hepatotoxic drug. Avoid entirely in existing liver disease. If the herb is used, obtain baseline and follow-up liver function tests and creatine phosphokinase, and stop immediately on any rise.
Digoxin, loop and thiazide diuretics, and corticosteroids
The seed carries a substantial free anthraquinone load and the drug is used traditionally to relax the bowels. Anthraquinone catharsis wastes potassium, and that loss is additive with diuretics and corticosteroids and dangerous in a digitalised patient.
Clinical note: Avoid in digitalised patients and in those on high-dose diuretics. Keep any course short and monitor potassium.
Roasted seed used as a coffee substitute (negro coffee, cafe negro)
The roasted seed is widely used as a coffee substitute across the tropics, which is a route of chronic, self-directed, high-volume exposure. Roasting is not a validated detoxification step for the anthraquinone fraction, and toxicity in animal feeding studies appears at seed loads of a few percent of the diet.
Clinical note: Ask patients from regions where the seed is drunk as coffee about this habit before adding any anthraquinone-containing herb, and advise against it in children, in pregnancy and in anyone with liver disease.
Evidence Tier
Strong evidence · 6 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
1
1 verified · 0 unverified
Randomized controlled trial
0
Other clinical trial
0
Observational / case report
0
In vitro / animal
5
2 verified · 3 unverified
Show 5 studies
- Association between children death and consumption of Cassia occidentalis seeds: Clinical and experimental investigations
- Interaction of anthraquinones of Cassia occidentalis seeds with DNA and Glutathione
- Toxicity Testing of Senna occidentalis Seed in Rabbits
- Experimental mitochondrial myopathy induced by chronic intoxication by Senna occidentalis seeds
- Sub-acute intoxication by Senna occidentalis seeds in rats
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
Association between children death and consumption of Cassia occidentalis seeds: Clinical and experimental investigations
Wistar rats were fed 0.5, 1 or 2 percent ground S. occidentalis seed in the diet for 28 days alongside clinical investigation of poisoning cases from northern India. The seed raised serum transaminases, alkaline phosphatase and lactate dehydrogenase with hepatic histopathological lesions; reduced grip strength with skeletal muscle vacuolisation and myopathy alongside raised creatinine and creatine phosphokinase; and produced neuronal damage with increased glial fibrillary acidic protein and decreased beta-tubulin III. Liver, muscle and brain were the target organs in both the animals and the children, and the authors conclude seed consumption is the main aetiological factor for the childhood hepatomyoencephalopathy.
Role of anthraquinones in Cassia occidentalis induced hepato-myo-encephalopathy
A systematic review of literature from 1956 to 2019 on the phytochemistry, toxicology and mechanism of toxicity of S. occidentalis. It concludes that the anthraquinones are the primary agents responsible for the hepato-myo-encephalopathy syndrome, acting through DNA binding, reactive oxygen species generation and enzyme inhibition, and producing hepatic necrosis with raised ALT, AST and LDH, muscle vacuolisation with raised creatine phosphokinase, and neuronal damage indexed by GFAP and beta-tubulin III. The review also notes the absence of diagnostic tests as a barrier to clinical management of poisoning.
Interaction of anthraquinones of Cassia occidentalis seeds with DNA and Glutathione
Fluorescence spectroscopy, UV-vis analysis, molecular docking and biochemical assay were used to study binding of the five seed anthraquinones to calf thymus DNA and glutathione. Emodin bound DNA most strongly (Ka = 3.854 x 10^4 L/mol/s), followed by aloe-emodin and rhein, while physcion and chrysophanol showed very low DNA binding and correspondingly lower cytotoxicity. Aloe-emodin and physcion appeared to form glutathione conjugates, and aloe-emodin and rhein oxidised glutathione to GSSG by 28 and 30 percent respectively, providing a mechanism for the differential toxicity of the individual anthraquinones.
Toxicity Testing of Senna occidentalis Seed in Rabbits
Rabbits received ground S. occidentalis seed at 1, 2, 3 or 4 percent of the ration for 30 days. Animals on the 4 percent ration gained less weight and died in the third week. Heart and liver were the main organs affected, with myocardial necrosis and centrilobular degeneration; cytochrome oxidase activity fell in the glycogenolytic fibres and muscle atrophy was confirmed morphometrically. Electron microscopy of liver cells showed dilated mitochondria with destruction of the internal cristae, the same mitochondrial lesion seen in the myopathy.
Experimental mitochondrial myopathy induced by chronic intoxication by Senna occidentalis seeds
Chronic feeding of S. occidentalis seed produced an experimental mitochondrial myopathy, establishing the muscle lesion of this plant as a primary mitochondrial injury rather than a secondary consequence of liver failure. This work underpins the modern understanding that the myopathy component of the human hepato-myo-encephalopathy syndrome is mitochondrial in origin.
Sub-acute intoxication by Senna occidentalis seeds in rats
A sub-acute rat feeding study of S. occidentalis seed characterising the dose-related organ damage produced over a short exposure period. It is part of the Brazilian series that established the seed as the toxic plant part and defined the hepatic and muscular lesions later recognised in the Indian childhood outbreaks.
Historical Texts
Jiu Huang Ben Cao
Ming dynasty, 1406Xian Dai Shi Yong Zhong Yao
Modern, twentieth centuryNan Ning Shi Yao Wu Zhi
Modern, twentieth centuryReferences
- Nirupam N, Sharma R, Chhapola V, Kanwal SK, Kumar V. Hepatomyoencephalopathy due to Cassia occidentalis Poisoning . The Indian Journal of Pediatrics (2012) [DOI]
- Barbosa-Ferreira M, Pfister JA, Gotardo AT, Maiorka PC, Gorniak SL. Intoxication by Senna occidentalis seeds in pregnant goats: Prenatal and postnatal evaluation . Experimental and Toxicologic Pathology (2011) [DOI]
- Calore EE, Weg R, Haraguchi M, Calore NMP, Cavaliere MJ, Sesso A. Mitochondrial metabolism impairment in muscle fibres of rats chronically intoxicated with Senna occidentalis seeds . Experimental and Toxicologic Pathology (2000) [DOI]
- Hatano T, Mizuta S, Ito H, Yoshida T. C-Glycosidic flavonoids from Cassia occidentalis . Phytochemistry (1999) [DOI]
- Lal J, Gupta PC. Physcion and phytosterol from the roots of Cassia occidentalis . Phytochemistry (1973) [DOI]
- Velez-Gavilan J. Senna occidentalis (coffee senna) . CABI Compendium (2016) [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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