White crystalline powder
(3β,25R)-17-Hydroxyspirost-5-en-3-yl 2-O-(6-deoxy-β-L-mannopyranosyl)-β-D-glucopyranoside/β-D-Glucopyranoside, (3β,25R)-17-hydroxyspirost-5-en-3-yl 2-O-(6-deoxy-α-L-mannopyranosyl)-/N1925/polyphyllin VI/β-D-Glucopyranoside, (3β,25R)-17-hydroxyspirost-5-en-3-yl 2-O-(6-deoxy-β-L-mannopyranosyl)-/(3β,25R)-17-Hydroxyspirost-5-en-3-yl 2-O-(6-deoxy-α-L-mannopyranosyl)-β-D-glucopyranoside
871.2±65.0 °C at 760 mmHg
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Polyphyllin VI (PPVI), a bioactive component derived from a traditional Chinese herb Paris polyphylla, exhibits potential antitumor activity against hepatocellular carcinoma, as well as breast and lung cancers. However, its effect on glioma remains unknown.
Five glioma cell lines (U251, U343, LN229, U87 and HEB) and an animal model were employed in the study. Anti-proliferation effects of PPVI were first determined using CCK-8 cell proliferation and clone formation assays, then reactive oxygen species (ROS), cell cycle progression and apoptosis effects measured by flow cytometry. The effect of PPVI on protein expression was quantified by Western blot analysis.
Data showed that PPVI inhibited the proliferation of glioma cell lines by modulating the G2/M phase. Additionally, incubation of cells with PPVI promoted apoptosis, autophagy, increased accumulation of ROS and activated ROS-modulated JNK and p38 pathways. On the other hand, N-acetyl cysteine, a ROS inhibitor, attenuated PPVI-triggered effects. Furthermore, JNK and p38 inhibitors ameliorated PPVI-triggered autophagy and apoptosis in glioma cells. In vivo assays showed that PPVI inhibited tumor growth of U87 cell line in nude mice.
Overall, these data suggested that PPVI might be an effective therapeutic agent for glioma.
© 2020 Liu et al.
apoptosis; autophagy; glioma; polyphyllin VI; reactive oxygen species
Polyphyllin VI Induces Apoptosis and Autophagy via Reactive Oxygen Species Mediated JNK and P38 Activation in Glioma.
Liu W1, Chai Y1, Hu L1, Wang J2, Pan X2, Yuan H3, Zhao Z3, Song Y3, Zhang Y1.
2020 Mar 13
Trillium tschonoskii Maxim (TTM), a traditional Chinese medicine, has been demonstrated to have a potent anti-tumor effect. Recently, polyphyllin VI (PPVI), a main saponin isolated from TTM, was reported by us to significantly suppress the proliferation of non-small cell lung cancer (NSCLC) via the induction of apoptosis and autophagy in vitro and in vivo. In this study, we further found that the NLRP3 inflammasome was activated in PPVI administrated A549-bearing athymic nude mice. As is known to us, pyroptosis is an inflammatory form of caspase-1-dependent programmed cell death that plays an important role in cancer. By using A549 and H1299 cells, the in vitro effect and action mechanism by which PPVI induces activation of the NLRP3 inflammasome in NSCLC were investigated. The anti-proliferative effect of PPVI in A549 and H1299 cells was firstly measured and validated by MTT assay. The activation of the NLRP3 inflammasome was detected by using Hoechst33324/PI staining, flow cytometry analysis and real-time live cell imaging methods. We found that PPVI significantly increased the percentage of cells with PI signal in A549 and H1299, and the dynamic change in cell morphology and the process of cell death of A549 cells indicated that PPVI induced an apoptosis-to-pyroptosis switch, and, ultimately, lytic cell death. In addition, belnacasan (VX-765), an inhibitor of caspase-1, could remarkably decrease the pyroptotic cell death of PPVI-treated A549 and H1299 cells. Moreover, by detecting the expression of NLRP3, ASC, caspase-1, IL-1β, IL-18 and GSDMD in A549 and h1299 cells using Western blotting, immunofluorescence imaging and flow cytometric analysis, measuring the caspase-1 activity using colorimetric assay, and quantifying the cytokines level of IL-1β and IL-18 using ELISA, the NLRP3 inflammasome was found to be activated in a dose manner, while VX-765 and necrosulfonamide (NSA), an inhibitor of GSDMD, could inhibit PPVI-induced activation of the NLRP3 inflammasome. Furthermore, the mechanism study found that PPVI could activate the NF-κB signaling pathway via increasing reactive oxygen species (ROS) levels in A549 and H1299 cells, and N-acetyl-L-cysteine (NAC), a scavenger of ROS, remarkably inhibited the cell death, and the activation of NF-κB and the NLRP3 inflammasome in PPVI-treated A549 and H1299 cells. Taken together, these data suggested that PPVI-induced, caspase-1-mediated pyroptosis via the induction of the ROS/NF-κB/NLRP3/GSDMD signal axis in NSCLC, which further clarified the mechanism of PPVI in the inhibition of NSCLC, and thereby provided a possibility for PPVI to serve as a novel therapeutic agent for NSCLC in the future.
NSCLC; ROS/NF-κB/NLRP3/GSDMD; polyphyllin VI; pyroptosis
Polyphyllin VI Induces Caspase-1-Mediated Pyroptosis via the Induction of ROS/NF-κB/NLRP3/GSDMD Signal Axis in Non-Small Cell Lung Cancer.
Teng JF1, Mei QB1, Zhou XG1, Tang Y1, Xiong R1, Qiu WQ1, Pan R2, Law BY3, Wong VK3, Yu CL2, Long HA1, Xiao XL1, Zhang F1, Wu JM1,4, Qin DL1,4, Wu AG1,4.
2020 Jan 13
Non-small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancers. Our previous studies have proven that Trillium tschonoskii Maxim. (TTM), a traditional Chinese medicine, possesses potent anti-tumor effect. However, the detailed components and molecular mechanism of TTM in anti-NSCLC are still unknown. In the present experiment, polyphyllin VI (PPVI) was successfully isolated from TTM with guidance of the anti-proliferative effect in A549 cells, and the cell death of PPVI treated A549 and H1299 cells was closely linked with the increased intracellular ROS levels. In addition, PPVI induced apoptosis by promoting the protein expression of Bax/Bcl2, caspase-3 and caspase-9, and activated autophagy by improving LC3 II conversion and GFP-LC3 puncta formation in A549 and H1299 cells. The mechanism study found that the activity of mTOR which regulates cell growth, proliferation and autophagy was significantly suppressed by PPVI. Accordingly, the PI3K/AKT and MEK/ERK pathways positively regulating mTOR were inhibited, and AMPK negatively regulating mTOR was activated. In addition, the downstream of mTOR, ULK1 at Ser 757 which downregulates autophagy was inhibited by PPVI. The apoptotic cell death induced by PPVI was confirmed, and it was significantly suppressed by the overexpression of AKT, ERK and mTOR, and the induced autophagic cell death which was depended on the Atg7 was decreased by the inhibitors, such as LY294002 (LY), Bafilomycin A1 (Baf), Compound C (CC) and SBI-0206965 (SBI). Furthermore, the mTOR signaling pathway was regulated by the increased ROS as the initial signal in A549 and H1299 cells. Finally, the anti-tumor growth activity of PPVI in vivo was validated in A549 bearing athymic nude mice. Taken together, our data have firstly demonstrated that PPVI is the main component in TTM that exerts the anti-proliferative effect by inducing apoptotic and autophagic cell death in NSCLC via the ROS-triggered mTOR signaling pathway, and PPVI may be a promising candidate for the treatment of NSCLC in future.
Copyright © 2019 Elsevier Ltd. All rights reserved.
Apoptosis; Arsenic trioxide (PubChem CID: 14888); Autophagy; Bafilomycin A1 (PubChem CID: 6436223); Camptothecin (PubChem CID: 24360); Compound C (PubChem CID: 11524144); Everolimus (PubChem CID: 6442177); Gefitinib (PubChem CID: 123631); LY294002 (PubChem CID: 3973); N-Acetyl-l-cysteine (PubChem CID: 12035); Paclitaxel (PubChem CID: 36314); Polyphyllin VI; Polyphyllin VI (PubChem CID: 71307571); ROS; Sirolimus (PubChem CID: 5284616); Temsirolimus (PubChem CID: 6918289); mTOR
Polyphyllin VI, a saponin from Trillium tschonoskii Maxim. induces apoptotic and autophagic cell death via the ROS triggered mTOR signaling pathway in non-small cell lung cancer.
Teng JF1, Qin DL2, Mei QB1, Qiu WQ1, Pan R3, Xiong R1, Zhao Y1, Law BY4, Wong VK4, Tang Y1, Yu CL3, Zhang F5, Wu JM6, Wu AG7.
Polyphyllin VI, an active saponin mainly isolated from traditional medicinal plant Paris polyphylla, possess anti-cancer activities. Polyphyllin VI induces G2/M cell cycle arrest and triggers apoptosis.