Herbs and plantsGorysz — the root that pharmacies abandoned too soon?
- Henryk Różański — Peucedanum – gorysz w praktycznej fitoterapii
- Research progress of the studies on the roots of Peucedanum praeruptorum dunn (Peucedani radix). · Pak J Pharm Sci 2015
- Peucedani Radix ameliorates bladder overactivity induced by partial bladder outlet obstruction via Nos3-mediated activation of the cGMP-PKG signaling pathway. · Phytomedicine 2026
- Attenuation of airway hyperreactivity and T helper cell type 2 responses by coumarins from Peucedanum praeruptorum Dunn in a murine model of allergic airway inflammation. · J Ethnopharmacol 2012
- Pyranocoumarin(+/-)-4'-O-acetyl-3'-O-angeloyl-cis-khellactone induces mitochondrial-dependent apoptosis in HL-60 cells. · Planta Med 2004
Gorysz is used for digestive problems, loss of appetite, cough, and disorders related to bile.
- Other reported uses include epilepsy, nervousness, stress, skin diseases, and catarrh of the respiratory tract.
- Historically, gorysz root was mentioned for epilepsy, while gorysz miarz was used for delirium tremens.
- A compound found in the rhizome of gorysz miarz was identified as a possible treatment for psoriasis and acne.
What the authors write
Gorysz błotny and gorysz miarz are used for digestive and bile disorders, epilepsy, nervousness, stress, skin diseases, and catarrh of the upper respiratory tract.
Gorysz infusion is used for loss of appetite, digestive problems, inflammation of the stomach and intestines, and cough.
In traditional medicine, gorysz root was mentioned as a treatment for epilepsy, while gorysz miarz was used for delirium tremens.
Imperatorin from the rhizome of gorysz miarz was identified as a possible treatment for psoriasis and acne.
Research from PubMed · Europe PMC
We selected 4 studies with the best, positive results. This is a selection, not a full review of all research.
Total number of studies on this topic in PubMed: 22.
The root of Peucedanum praeruptorum is traditionally used for cough with thick phlegm, shortness of breath, dry cough, and upper respiratory tract infections.
Aim of the study: As a commonly used traditional Chinese medicine, Peucedani Radix (Qian-hu in Chinese), which consists of the dried roots of Peucedanum praeruptorum Dunn, has a long history of use in traditional medicine for treating cough with thick sputum and dyspnea, nonproductive cough, and upper airway infections.
Results: Crude extracts and pure compounds from Peucedani Radix have shown a wide range of pharmacological activities in vitro and in vivo, including vasorelaxant, cardioprotective, hepatoprotective, antitumor, and antiplatelet effects. In contrast to the well-defined chemical constituents and activities, absorption, pharmacokinetics, and metabolism have rarely been characterized. However, further research is needed to develop new drugs and therapies for various diseases, especially cardiovascular disorders. Overall, this review of the phytochemistry, chemical analysis, pharmacological evaluation, and pharmacokinetic profile of Peucedani Radix will provide useful information for further studies and commercial development of this herbal medicine.
“Not stated” does not mean nobody paid — the database does not always record it.
In a rat study, Peucedani Radix root alleviated symptoms of overactive bladder caused by an obstruction to urine flow.
Aim of the study: Overactive bladder (OAB) is a common clinical challenge worldwide, with few effective treatments. This study aimed to investigate the therapeutic effects and underlying molecular mechanisms of Peucedani Radix (PR), the dried root of Peucedanum praeruptorum Dunn, in a rat model of overactive bladder (OAB) induced by partial bladder outlet obstruction (pBOO), and to clarify the roles of its active components.
Results: PR significantly reduced bladder overactivity, detrusor hypercontractility, and the abnormal smooth muscle-to-collagen ratio in rats with pBOO. Integrated transcriptomic and network pharmacological analyses identified the cGMP-PKG signaling pathway as the core pathway and Nos3 as a potential key molecular target. PR was also confirmed to increase Nos3 expression and activate the cGMP-PKG pathway. In addition, dl-praeruptorin A was identified as PR’s main bioactive component, which binds directly to Nos3. Cell experiments showed that dl-praeruptorin A inhibited contractions of bladder smooth muscle cells caused by hydrostatic pressure through Nos3-mediated activation of the cGMP-PKG pathway; this effect was abolished when Nos3 was knocked down. Corresponding changes were observed in intracellular nitric oxide levels, Nos3 expression, and proteins related to the cGMP-PKG pathway.
“Not stated” does not mean nobody paid — the database does not always record it.
Compounds from Peucedanum praeruptorum root reduced airway hyperreactivity and inflammation in mice with allergic inflammation.
Aim of the study: The potential of coumarins from PPD (CPPD) as an anti-asthma agent was investigated.
Results: Compared with the model group, CPPD significantly reduced airway hyperreactivity and eosinophilic airway inflammation, improved lung lesions, reduced levels of IL-4, IL-5, and IL-13 in BALF and OVA-specific IgE in serum, inhibited EPO activity in the lungs, and increased levels of IL-10 and IFN-γ in BALF, as well as the percentage of CD4(+)CD25(+)Foxp3(+) regulatory T cells in the spleen. CPPD can significantly suppress OVA-induced airway inflammation, airway hyperreactivity, and the Th2-dominant response in mice, showing strong potential as a treatment for allergic asthma.
“Not stated” does not mean nobody paid — the database does not always record it.
A compound isolated from Peucedanum praeruptorum root induced apoptosis in leukemia cells in laboratory conditions.
Aim of the study: The pyranocoumarin (+)-4'-O-acetyl-3'O-angeloyl-cis-khellactone (PC), isolated from Radix Peucedani (the root of Peucedanum praeruptorum Dunn), showed a dose-dependent effect at 10–30 pg/mL, causing apoptotic DNA and nuclear fragmentation in HL-60 cells. After 24 hours of PC treatment, mitochondrial membrane potential and cytochrome c were lost.
Results: The pan-specific caspase inhibitor ZVAD-fmk abolished PC-induced apoptosis, whereas the caspase-8 inhibitor IETD-fmk had no effect, suggesting involvement of the caspase 9 pathway. PC caused a transient increase in phospho-ERK lasting 2 to 12 hours and activation of JNK lasting 72 hours. Pre-treatment with the MEK inhibitor PD98059, which suppresses ERK activation, paradoxically promoted PC-induced mitochondrial cytochrome c release, procaspase-3 and -8 cleavage, and increased apoptosis. Our results show that PC triggers mitochondria-mediated apoptosis in HL-60 cells and that ERK and JNK signaling pathways are involved in the process.
“Not stated” does not mean nobody paid — the database does not always record it.
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