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Paris saponin VII


  • Brand : BIOFRON

  • Catalogue Number : BF-C4007

  • Specification : 98%(HPLC)

  • CAS number : 68124-04-9

  • Formula : C51H82O21

  • Molecular Weight : 1031.21

  • PUBCHEM ID : 176233

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

roots of Paris polyphylla

Structure Type



Standards;Natural Pytochemical;API




(3β,25R)-17-Hydroxyspirost-5-en-3-yl 6-deoxy-α-L-mannopyranosyl-(1->2)-[6-deoxy-α-L-mannopyranosyl-(1->4)-6-deoxy-α-L-mannopyranosyl-(1->4)]-β-D-glucopyranoside/β-D-Glucopyranoside, (3β,25R)-17-hydroxyspirost-5-en-3-yl O-6-deoxy-α-L-mannopyranosyl-(1->2)-O-[O-6-deoxy-α-L-mannopyranosyl-(1->4)-6-deoxy-α-L-mannopyranosyl-(1->4)]-/Paris saponin VII




1.5±0.1 g/cm3



Flash Point

Boiling Point

Melting Point



InChl Key


WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:68124-04-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




To find the effect of Paris saponin VII (PS VII)-mediated PI3K/AKT/MAPK signaling pathway on the sensitivity of ADR-resistant HepG2 cell (HepG2/ADR) cells to ADR. The proliferation inhibitory rates were detected by using MTT assay. Flow cytometry was employed to examine the intracellular accumulation of ADR. The expressions of drug-resistant genes (P-gp, MRP and BCRP) were detected by qRT-PCR, cell apoptosis by Annexin-V-FITC/PI staining, and the expressions of drug-resistance-related proteins, apoptosis-related proteins, and PI3K/AKT/MAPK pathway-related proteins were determined by Western blotting. HepG2/ADR and HepG2 cells treated with PS VII (0.88, 1.32, 1.98, and 2.97 μM) for 48 hours showed increased proliferation inhibitory rate in a dose-dependent manner. HepG2/ADR cells treated PS VII (0.88, 1.32, 1.98 μM) for 48 hours showed decreased IC50 of ADR. Compared with HepG2/ADR cells treated with ADR (5 nM), those treated with PS VII (≤1.98 μM) and ADR (5 nM) showed enhanced ADR accumulation, decreased drug-resistant gene expressions, increased cell apoptosis with unregulated Bax and cleaved caspase-3 and downregulated Bcl-2, as well as the inhibition of PI3K/AKT/MAPK pathway. Moreover, the combination of ADR (5 nM), PS VII (1.98 μM), and LY294002 (PI3K/AKT inhibitor, 20 μM)/SB203580 (P38 inhibitor, 20 μM) for 48 hours could further decreased the HepG2/ADR cell viability, but induced cell apoptosis, accompanying with the decreased expressions of drug-resistant genes. PS VII could downregulate the expressions of drug-resistance genes, increase intracellular accumulation of ADR, promote cell apoptosis, and enhance the sensitivity of HepG2/ADR cells to ADR via PI3K/AKT/MAPK.

© 2019 The Authors. The Kaohsiung Journal of Medical Sciences published by John Wiley & Sons Australia on behalf of Kaohsiung Medical University.


ADR; HepG2; PI3K/AKT/MAPK; Paris saponin VII; hepatocellular carcinoma


Paris saponin VII enhanced the sensitivity of HepG2/ADR cells to ADR via modulation of PI3K/AKT/MAPK signaling pathway.


Tang GE1, Niu YX1, Li Y1, Wu CY1, Wang XY1, Zhang J1.

Publish date

2020 Feb




Trillium tschonoskii Maxim, a perennial herb of the Trilliaceae, has been widely used to treat inflammation, hypertension and cancer. We investigated Paris saponin VII’s (PS VII), isolated from Trillium tschonoskii Maxim, function in mediating autophagy and apoptosis in NSCLC cells.

We treated various NSCLC cells with different concentrations of PS Ⅶ and then measure the cell apoptosis by using flow cytometry assays and western blot. Autophagy were investigated by using western blot, transmission electron microscopy and immunofluorescence analysis. We also use a xenograft model of nude mice to measure the effect of PS Ⅶ in vivo.

Treatment with PS Ⅶ significantly inhibit NSCLC cell growth, especially for A549 (IC50 = 1.53 μM). Moreover, PS VII induces caspase-dependent apoptosis and autophagy through AMPK-ULK1 pathway. After blocking autophagy by 3-methyladenine (3-MA), PS VII induced cell death was significantly increased. In vivo, the co-treatment with PS VII and 3-MA dramatically inhibited A549 tumor growth in immune deficient mice and has similar inhibition rates as cisplatin group.

Our results suggest that a combination of PS VII and autophagy inhibitor may be a potential anticancer strategy in the NSCLC therapy.

Copyright © 2019 Elsevier B.V. All rights reserved.


AMPK; Apoptosis; Autophagy; NSCLC


Paris saponin VII extracted from Trillium tschonoskii induces autophagy and apoptosis in NSCLC cells.


Qian S1, Tong S2, Wu J3, Tian L4, Qi Z5, Chen B6, Zhu D7, Zhang Y8.

Publish date

2020 Feb 10




Metastasis is the primary cause of mortality in osteosarcoma. Targeting metastasis is a major strategy in osteosarcoma treatment. As a traditional Chinese medicine, Trillium tschonoskii Maxim has been widely used in the therapy of various diseases, including cancer. However, currently there is no evidence regarding the anti‑metastasic effect of Paris saponin VII (PS VII), which is extracted from Trillium tschonoskii Maxim, on osteosarcoma cells and its underling mechanisms. The present study aimed to examine the effect of PS VII on the migration and invasion of osteosarcoma cells. Viability and proliferation of osteosarcoma cells were examined by MTT assay. Migration and invasion of osteosarcoma cells was then detected using scratch wound healing assays and Transwell assays, respectively. Additionally, the expression of matrix metalloproteinase (MMP)‑2 and ‑9 was determined at the mRNA and protein level following treatment with PS VII. Mitogen‑activated protein kinase (MAPK) expression was also detected by western blot analysis. Finally, an inhibitor of p38 MAPK was used to verify the effect of PS VII on the expression of MMP‑2 and ‑9, as well as the migration and invasion osteosarcoma cells. This demonstrated that the proliferation, migration and invasion of the osteosarcoma cells were suppressed following treatment with PS VII. PS VII downregulated the expression of MMP‑2 and ‑9 in a dose‑ and time‑dependent manner. PS VII also exerted its ability to downregulate the phosphorylation of p38 MAPKs. Furthermore, by using a p38 inhibitor, SB203580, the role of PS VII in MMP‑2 and ‑9 expression and osteosarcoma cell invasion was revealed. Taken together, these results demonstrated that PS VII suppresses the migration and invasion of osteosarcoma cells via the p38 MAPK signaling pathway.


Paris saponin VII suppresses osteosarcoma cell migration and invasion by inhibiting MMP‑2/9 production via the p38 MAPK signaling pathway.


Cheng G1, Gao F2, Sun X1, Bi H1, Zhu Y2.

Publish date

2016 Oct

Description :

Paris saponin VII (Chonglou Saponin VII) is a steroidal saponin isolated from the roots and rhizomes of Trillium tschonoskii Maxim. Paris saponin VII-induced apoptosis in K562/ADR cells is associated with Akt/MAPK and the inhibition of P-gp. Paris saponin VII attenuates mitochondrial membrane potential, increases the expression of apoptosis-related proteins, such as Bax and cytochrome c, and decreases the protein expression levels of Bcl-2, caspase-9, caspase-3, PARP-1, and p-Akt. Paris saponin VII induces a robust autophagy in K562/ADR cells and provides a biochemical basis in the treatment of leukemia[1].