Abstract Given the rising global incidence of inflammatory bowel disease (IBD) and limited treatment options, probiotic efficacy is hindered by poor gastrointestinal survival. This study developed a self-coating biofilm technology to encapsulate the probiotic Bacillus amyloliquefaciens C-1 and yield cC-1. Biofilm-modified cC-1 exhibited a more negative zeta potential (-22.53 mV) compared to uncoated C-1 (-19.60 mV), representing a decrease of 2.93 mV decreased zeta potential, and it exhibited orders of magnitude higher survival than uncoated cells under simulated gastric acid (80.51% vs . 0.33%) and bile salt (84.32% vs . 1.64%). In DSS-induced colitis mice, oral administration of 10⁹ CFU cC-1 for 14 days significantly alleviated symptoms, reduced colon shortening and restored mucosal integrity. Mechanistically, cC-1 effectively downregulated pro-inflammatory cytokines (TNF- α , IL-1 β , IL-6 and IFN- γ ) in colon tissues; reshaped the diversity of gut microbiota by enriching beneficial Bacteroides ; restored linoleic acid and glycerophospholipid metabolism, and suppressed expression of NF- κ B signaling and cell adhesion molecule. Transcriptomic analysis confirmed that cC-1 reinstated host-microbe metabolic interactions with suppressed inflammatory pathways. This biofilm self-coating strategy substantially enhances probiotic gastrointestinal tolerance and exerts therapeutic effects through a multi-targeted mechanism (anti-inflammation, barrier repair, microbiota modulation, and metabolic reprogramming), offering a scalable and promising formulation for nutritional intervention in IBD.

BACKGROUND:Metabolic-associated fatty liver disease (MAFLD), particularly advanced metabolic dysfunction-associated steatohepatitis (MASH), leads to irreversible liver damage. Specnuezhenide (SPE), naturally isolated from Ligustrum lucidum Ait, has been demonstrated to exert hepatoprotective effects. However, its functional role and underlying mechanisms in MAFLD remain poorly understood. PURPOSE:This study investigated the therapeutic effects and potential mechanism of SPE on MAFLD. METHODS:MAFLD mice induced by high-fat diet (HFD) were employed to assess SPE's therapeutic effects in vivo. The impact of SPE on gut microbiota was analysed by 16S rRNA sequencing. RNA-seq analysis was conducted to uncover SPE's molecular mechanisms. Complementary in vitro investigations utilized FFA-treated HepG2 cells to systematically examine SPE's cellular-level impacts and regulatory pathways. RESULTS:The results indicated that SPE could improve hepatic steatosis, liver injury and oxidative stress in MAFLD mice. SPE treatment also affected the diversity of gut microbiota and altered their composition by decreasing the Firmicutes/Bacteroidetes (F/B) ratio. The results of 16S rRNA sequencing, RNA-seq and Western blot analysis indicated that the effect of SPE on MAFLD was related to fatty acid beta-oxidation and the PPARα signalling pathway. Moreover, in HepG2 cells, SPE reduced FFA-induced lipid accumulation and oxidative stress, which was dependent on PPARα up-regulation. CONCLUSION:This is the first study to demonstrate that SPE alleviates MAFLD and is associated with modulation of gut microbiota composition and activation of the PPARα signalling pathway. Our findings suggest a potential link between gut microbiota remodelling and PPARα-mediated fatty acid oxidation, highlighting its potential as a therapeutic candidate for MAFLD.

Metabolic dysfunction-associated steatohepatitis (MASH) has emerged as the primary contributor to the increasing incidence and mortality rates linked to cirrhosis and hepatocellular carcinoma globally, while the availability of clinical treatment drugs remains severely limited. Ecliptasaponin A (EA), naturally isolated from Ecliptae Herba, possesses multiple biological activities. However, the effects of EA on MASH remain unclear. This study aimed to explore the roles of EA in MASH and its engaged mechanisms. Two established NASH animal models, non-obese MASH induced by methionine-choline-deficient (MCD) dietary administration and obese MASH developed through high-fat/high-cholesterol (HFHC) feeding were employed to assess EA's therapeutic effects in vivo. RNA-seq analysis was conducted to uncover EA's molecular mechanisms. Complementary in vitro investigations utilized LPS-treated BMDMs and THP1 cells, and TGF-β1-activated LX-2 hepatic stellate cells to systematically examine EA's cellular-level impacts and regulatory pathways. Oral administration of EA demonstrated dose-responsive therapeutic effects against MCD/HFHC-induced MASH. The compound effectively attenuated hepatic steatosis, inflammatory responses, and fibrotic progression in experimental models through dual modulation of NLRP3 and YAP signaling pathways. Mechanistic studies revealed EA specifically suppressed NLRP3 inflammasome activation in BMDMs without affecting AIM2 or NLRC4 inflammasomes, effectively blocking cytokine secretion, pyroptotic cell death, caspase-1 activation, and inflammasome complex formation. Molecular interactions analysis confirmed EA directly binds to NLRP3, disrupting inflammasome assembly. In LX-2 cells, EA suppressed TGF-β1-induced COL1A1 and α-SMA expression while reducing YAP protein levels. Genetic silencing or pharmacological inhibition of YAP failed to potentiate EA's anti-fibrotic effects on α-SMA suppression, Collagen I expression, or YAP-regulated gene transcription. Molecular docking and SPR showed that EZ could directly bind to NLRP3 and YAP. These findings reveal novel perspectives on the natural compound Ecliptasaponin A, demonstrating its dual-targeting capability against both NLRP3 inflammasome activation and YAP signaling cascades. This discovery highlights its potential as a promising therapeutic agent for mitigating MASH.

Glioma remains a critical challenge in neuro-oncology due to highly invasive behavior and limited treatment options. Saponins, a structurally diverse class of natural glycosides, have shown great potential as anti-glioma agents owing to their significant bioactivity and multi-target pharmacological properties. This review systematically summarizes the cytotoxicity of saponin compounds with anti-glioma activity, focuses on the analysis of their structure-activity relationships (SARs), elaborates in detail on the anti-glioma mechanisms of action exerted by different saponins, and corresponding solutions faced by saponins in clinical application. Saponins with anti-glioma activity are categorized into steroidal and triterpenoid types, and the key structural features and functional groups responsible for their efficacy are elucidated. Furthermore, we comprehensively summarize the core mechanisms by which saponins exert anti-glioma effects, including cell cycle arrest, apoptosis induction, suppression of invasion and migration, anti-angiogenesis, autophagy regulation, and reversal of drug resistance. Combined with the structural characteristics of saponins, we further discussed the bottleneck problems faced by this class of compounds in the process of drug development, as well as the targeted coping strategies. This study not only strengthens the theoretical foundation of saponins as anti-glioma lead compounds but also establishes a rational framework for their structural optimization and development into novel therapeutics.

ETHNOPHARMACOLOGICAL RELEVANCE:Erzhi pills (EZP), as a traditional Chinese herbal prescription, have protective effects against various forms of liver injury. However, the therapeutic potential, bioactive ingredients and mechanism of action of EZP for metabolic dysfunction-associated steatohepatitis (MASH) have not been completely elucidated. AIM OF THE STUDY:This research aimed to evaluate the therapeutic effect of EZP and its bioactive compounds on MASH. METHODS:Two typical animal models of MASH, mice fed a methionine-choline-deficient (MCD) diet (representing non-obese MASH) and mice fed a high-fat and high-cholesterol diet (HFHC) (representing obese MASH), were used to investigate the effect of EZP on MASH in vivo. Transcriptomic and proteomic analysis were performed to elucidate the under lying mechanisms of EZP. The compositional analysis of EZP in MASH mice was conducted using UPLC-Q-Exactive-Orbitrap-MS. Free fatty acid (FFA)-stimulated HepG2 cells and transforming growth factor β1 (TGF-β1)-activated LX-2 cells were applied to further explore the effects and mechanisms of bioactive compounds from EZP. RESULTS:Our results indicate that the EZP mitigates hepatic lipid buildup, insulin resistance, inflammation, apoptosis, and fibrosis in different diet-induced MASH mice. Through multiomic analyses, UPLC-Q-Exactive-Orbitrap-MS analysis and molecular docking, we have identified that EZP exerts therapeutic effects on MASH involves activation of PPARα and PI3K/AKT/FoxO1 pathways, and inhibition of NLRP3, p53, and yes-associated protein (YAP) signaling pathways. It had been established that wedelolactone (wed), specnuezhenide (Spe), salidroside (Sal), and echinocystic acid-3-o-glucoside (Ech) served as the primary bioactive compounds in EZP for its therapeutic effect against MASH. In vitro experiments have confirmed that Spe, Sal, and Ech mitigate lipid accumulation by activating PPARα. Additionally, Spe and Sal improve insulin resistance through the activation of the PI3K/AKT/FoxO1 signaling pathway. Furthermore, Wed, Sal, and Ech inhibit the NLRP3 inflammasome and p53 signaling pathways, thereby reducing inflammatory markers and providing anti-apoptotic effects. Moreover, Wed and Ech inhibit the activation of hepatic stellate cells (HSCs) by blocking the YAP signaling pathway. Notably, Sal and Ech were the primary bioactive components of EZP, and their combined anti-MASH efficacy was comparable to that of EZP. CONCLUSION:This study is the comprehensive elucidation of the active ingredients and mechanism of action behind EZP in its anti-MASH properties. EZP, as well as the combination of Sal and Ech are potential treatment for MASH that targets multiple signaling pathways.

Malignant gliomas are devastating tumors that frequently kill patients within 1 year of diagnosis. Diffuse invasion is a major obstacle to cure, which allows tumor to escape from complete surgical resection as well as chemotherapy and radiotherapy. Therefore, the development of new chemotherapeutic agent that inhibiting the infiltrative growth of glioma is urgently needed. Culcita novaeguineae-3 (CN-3) is a marine-derived steroidal saponin which exhibit significant cytotoxicity to glioma cells. This study was designed to confirm the effect of CN-3 on glioma and to further clarify its mechanism of action. The experimental results showed that CN-3 could significantly inhibit the proliferation, invasion and migration of glioma cells in vitro and in vivo. CN-3 could down-regulate the expression of high mobility group protein A1 (HMGA1), to inhibit the infiltrative growth of glioma cells. Furthermore, the metastatic mobility was significantly reduced in HMGA1 knockout glioma cells. Moreover, miR-4465 was confirmed to target and reduce HMGA1 expression. In addition, CN-3 could upregulate the expression of miR-4465 in cells, thereby inhibiting migration and invasion of glioma cells. These results elucidate the mechanism by which CN-3, a steroidal saponin from the sea, may inhibit the invasive behavior of glioma cells through the miRNA-4465/HMGA1/NF-κB pathway, which also raise the prospect of using CN-3 as a chemotherapeutic agent to prevent glioma invasive growth.

Since ancient times, plants have provided humans with important bioactive compounds for the treatment of various diseases. Nine compounds were isolated from the roots and rhizomes of Caulophyllum robustum (a plant in the family Panaxaceae), including two new saponins C. Spanion A and C. Spanion B (1-2) and seven known saponins (3-9). The cytotoxicity of these compounds on human cancer cell lines was analyzed using MTT method. Compounds 6 and 9 exhibit cytotoxicity towards these three types of human cancer cells (<10 μM). By utilizing the SEA platform for target prediction, a common tumor related target CD81 was identified. The molecular docking of saponins 1, 2, 6, and 9 with CD81 protein showed strong binding affinities ranging from -4.5 to -7.1 kcal/mol. Research has shown that these compounds can become potential anti-tumor drugs. Further research is still recommended to understand its exact molecular mechanism and toxicological effects.

Endometriosis (EMs) with anxiety/depression is a common comorbidity of EMs, yet effective treatments are still lacking. Leaves of Paeonia suffruticosa Andr. (PSL) have potential therapeutic effects on EMs and their associated psychiatric disorders. In this study, 57 chemical compounds were identified using Global Natural Products Social Molecular Networking (GNPS) and semi-preparative HPLC. Network pharmacology analysis revealed that these compounds shared 68 common targets with the disease, primarily enriched in the PI3K/AKT signaling pathway. Protein-protein interaction analysis identified TNF, IL-6, ESR1, AKT1, and TP53 as core targets. Molecular docking confirmed that apigenin, quercetin, kaempferol, luteolin, and isorhamnetin exhibited strong binding affinities with these core targets. In conclusion, PSL may exert beneficial effects in treating EMs with anxiety/depression by modulating the PI3K/AKT signaling pathway through key targets including TNF, IL-6, ESR1, AKT1, and TP53.

Objective: Paridis Rhizoma (Chonglou in Chinese), a traditional Chinese herbal medicine, has been shown have strong anti-tumor effects. Paris saponin VII (PSVII), an active constituent isolated from Paridis Rhizoma, was demonstrated to significantly suppress the proliferation of BxPC-3 cells in our previous study. Here, we aimed to elucidate the anti-pancreatic ductal adenocarcinoma (PDAC) effect of PSVII and the underlying mechanism. Methods: Cell viability was determined by CCK-8, colony formation, and cell migration assays. Cell apoptosis and reactive oxygen species (ROS) production were measured by flow cytometry with annexin V/propidine iodide (Annexin V/PI) and 20,70-dichlorodihydrofluorescein diacetate (DCFH-DA), respectively. Pyroptosis was evaluated by morphological features, Hoechst 33342/PI staining assay, and release of lactate dehydrogenase (LDH). JC-1 fluorescent dye was employed to measure mitochondrial membrane potential. Western blotting and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) were used to determine the levels of proteins or mRNAs. The effect in vivo was assessed by a xenograft tumor model. Results: PSVII inhibited the viability of PDAC cells (BxPC-3, PANC-1, and Capan-2 cells) and induced gasdermin E (GSDME) cleavage, as well as the simultaneous cleavage of Caspase-3 and poly (ADP-ribose) polymerase 1 (PARP). Knockdown of GSDME shifted PSVII-induced pyroptosis to apoptosis. Additionally, the effect of PSVII was significantly attenuated by Z-Asp(OMe)-Glu(OMe)-Val-Asp(OMe)-fl uoromethylketone (Z-DEVD-FMK), on the induction of GSDME-dependent pyroptosis. PSVII also elevated intracellular ROS accumulation and stimulated Bax and Caspase-3/GSDME to conduct pyroptosis in PDAC cells. The ROS scavenger N-acetyl cysteine (NAC) suppressed the release of LDH and inhibited Caspase-9, Caspase-3, and GSDME cleavage in PDAC cells, ultimately reversing PSVII-induced pyroptosis. Furthermore, in a xenograft tumor model, PSVII markedly suppressed the growth of PDAC tumors and induced pyroptosis. Conclusion: These results demonstrated that PSVII exerts therapeutic effects through Caspase-3/GSDMEdependent pyroptosis and may constitute a novel strategy for preventing chemotherapeutic resistance in patients with PDAC in the future. (c) 2024 Tianjin Press of Chinese Herbal Medicines. Published by ELSEVIER B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Liver fibrosis is a representative scarring response that can ultimately lead to liver cancer. However, relevant antifibrotic drugs for the effective treatment of liver fibrosis in humans have not yet been identified. Chikusetsusaponin IVa (CS-IVa) is derived from natural products and exhibits multiple biological activities; however, its efficacy and potential mechanism of action against liver fibrosis remains unclear. This study aimed to examine the antifibrotic properties and potential mechanisms of action of CS-IVa. We constructed two mature mouse models (CCl4 challenge and bile duct ligation) to evaluate the antifibrotic properties of CS-IVa in vivo. Proteomics analysis and transforming growth factor β1 (TGF-β1)-activated LX-2 cells were used to elucidate the potential effects and mechanisms. Molecular docking, surface plasmon resonance (SPR), and cellular thermal shift assay (CETSA) were used to detect the affinity and binding between CS-IVa and its target. We found that CS-IVa significantly alleviated liver fibrosis and injury by downregulating yes-associated protein (YAP) and tafazzin (TAZ) expression. In an in vitro model, CS-IVa suppressed TGF-β1-induced hepatic stellate cell (HSC) activation, as well as the mRNA and protein expression of COL1A1, α-SMA, YAP, and TAZ. Moreover, specific knockdown or inhibition of YAP did not enhance the suppressive effect of CS-IVa on HSC activation or fibrosis-associated protein expression. Molecular docking, SPR, and CETSA showed that CS-IVa could directly bind to YAP. These findings demonstrated that the administration of CS-IVa effectively alleviated liver fibrosis by suppressing the YAP/TAZ pathways. In addition, CS-IVa could directly bind to YAP and act as a YAP inhibitor.

ETHNOPHARMACOLOGICAL RELEVANCE:Ziziphi Spinosae Semen (ZSS), the dried mature seed of Ziziphus jujuba Mill. var. spinosa (Bunge) Hu ex H.F. Chou, is a classic traditional Chinese medicine (TCM) with a clinical application history of over two millennia. The host plant is mainly distributed in the tropical and subtropical regions of Asia and America. It was first recorded in Shen Nong's Herbal Classic; in TCM theory, ZSS is characterized by a sweet and sour taste, a neutral nature, and tropism for the Liver, Gallbladder, and Heart Meridians, and possesses the effects of nourishing the heart and replenishing the liver, calming the mind and tranquilizing the spirit, astringing sweating, and promoting the production of body fluids. These traditional applications provide a crucial foundation and direction for ethnopharmacological research. AIM OF THE REVIEW:The botanical characteristics, traditional and modern clinical applications, phytochemistry, pharmacological activity, and quality marker (Q-marker) prediction of ZSS are reviewed. It aims to address the limitations of traditional quality control and achieve the transition from "single-component detection" to "association with overall efficacy". MATERIALS AND METHODS:Available publications about ZSS were collected by searching library and electronic databases, including PubMed, CNKI, Web of Science, Google Scholar, relevant TCM journals, and classic works. RESULTS:Modern phytochemical and pharmacological studies show that ZSS contains 155 components, including terpenoids, steroids, flavonoids, alkaloids, fatty acids and volatile oils, and other constituents. Among these compounds, triterpenoid jujuboside A and flavonoid spinosin have attracted widespread attention for their diverse pharmacological activities, while other components in ZSS also contribute to its efficacy by exerting sedative and hypnotic, anti-anxiety, anti-Alzheimer's disease, and cardioprotective effects by regulating neurotransmitters, other neural pathways, and the intestinal flora. Through Q-marker predictive analysis revealed that jujuboside A, jujuboside B, spinosin, and 6‴-feruloylspinosin from ZSS are potential Q-markers. CONCLUSIONS:Although ZSS has therapeutic potential, the current quality control standards for ZSS are still insufficient. The Chinese Pharmacopoeia (2025 Edition) only relies on the quantification of jujuboside A and spinosin, failing to reflect their overall quality-this is an important limitation of the multi-component synergy principle of TCM. To address this gap, a novel predictive Q-marker model is proposed to integrate multi-dimensional data and establish a powerful and scientific quality assessment framework. By prioritizing bioactive ingredients with traceable efficacy and utilizing advanced analytical techniques, this work advances the standardization of ZSS, highlighting its significance for the modernization of TCM and evidence-based clinical applications.

Objectives:The Sorbin and SH3 domain containing 1 (SORBS1), a protein linked to insulin signaling CBL interaction, was investigated for its role in pancreatic cancer apoptosis. This study explored polyphyllin H (PPH)'s ability to restore SORBS1-knockdown-mediated repair functions. Methods:PANC-1 cells were divided into Blank, overexpression (OE), and knockdown groups. CCK-8 assays assessed proliferation and drug toxicity. Western blot and flow cytometry analyzed SORBS1 levels and PPH effects. Comet assays quantified DNA damage. Subcutaneous xenograft tumors in nude mice (Blank vs. knockdown) were treated with PPH to evaluate in vivo efficacy. SORBS1-H2AX gene correlation was analyzed Spearman rank clustering (p < 0.05). Results:PPH suppressed pancreatic cancer growth in vitro/vivo, but its efficacy was attenuated by SORBS1 downregulation. Clinically, low SORBS1 correlated with poor prognosis. SORBS1 knockdown promoted tumor proliferation and reduced PPH-induced apoptosis. While PPH decreased tumor volume in both Blank and knockdown groups compared to controls, SORBS1 knockdown diminished PPH's inhibitory effects. Mechanistically, SORBS1 depletion mitigated PPH-triggered DNA damage, circumventing G2/M arrest by modulating WEE1, Cyclin A2, CDK1, and Cyclin B1, thereby impairing apoptosis. Conclusion:SORBS1 knockdown counteracts PPH-mediated S/G2 arrest and apoptosis by alleviating DNA damage in pancreatic cancer. These findings highlight SORBS1 as a critical modulator of PPH's therapeutic potential, linking its expression to chemoresistance mechanisms.

Four new polyhydroxylated steroidal saponins, parisverticillatosides A-D (1-4), together with four known spirostanol saponins (5-8) were isolated from the roots of Paris verticillata. Their structures were elucidated on the basis of extensive spectroscopic analysis and chemical evidences. The discovery of the new compounds 1-4 extended the diversity and complexity of this spirostanol saponin family. The saponins 5 and 6 exhibited cytotoxicities against two human glioma cell lines.

The phytochemical investigation on the rhizomes of Paris yunnanensis Franch. resulted in the discovery and characterisation of six compounds, including two new saponins named parisyunnanosides M-N (1-2), and four known ones (3-6). The structures of isolated compounds were determined by spectroscopic data analysis and chemical methods. Compound 2 is a pregnane-type saponin with a special α,β-unsaturated carboxylic acid moiety at C-17, which is first discovered in genus Paris. The anti-inflammatory activity of the isolated compounds was assessed in vitro. The results demonstrated that compounds 3 and 4 could significantly inhibit the production of NO which was induced by LPS in RAW 264.7 cells with IC50 values of 0.67 ± 0.17 μM and 0.85 ± 0.12 μM, respectively.

Two previously undescribed cholestanol saponins, parpetiosides F - G ( 1 - 2 ), and six known analogs ( 3 - 8 ) were isolated from the rhizomes of Paris fargesii var. petiolata . Their structures were elucidated by extensive spectroscopic data analysis and chemical methods. Compound 1 was a rare 6/6/6/5/5 fused-rings cholestanol saponin with disaccharide moiety linked at C-26 of aglycone which was hardly seen in genus Paris . All of these compounds were discovered in this plant for the first time. In addition, the cytotoxicities of saponins (1 - 8) against three human cancer cell lines (U87, HepG2 and SGC-7901) were evaluated by CCK-8 method, and saponins 5 - 8 displayed certain cytotoxicities. The strong interactions between saponins 5 - 8 and SCUBE3, an oncogene for glioma cells, were displayed by molecular docking.

The phytochemical constituent investigation on the 70 % ethanol extract of the rhizomes of Tupistra chinensis Baker resulted in the isolation of three new steroidal saponins which were named tuchinosides A–C ( 1 – 3 ). Their structures were determined by extensive spectrum analysis and chemical evidence, especially 2D NMR and HR-ESI-MS techniques. In addition, the cytotoxicity of compounds 1–3 against several human cancer cell lines was evaluated.

目的 探讨重楼皂苷Ⅵ(PPⅥ)对脑胶质瘤细胞增殖和凋亡的影响及潜在机制.方法 以人脑胶质瘤LN229细胞为对象,采用MTT法检测不同浓度PPⅥ[0(对照组)、1、2、4、8、16、32、64 μmol/L]作用不同时间(24、48、72 h)后的细胞存活率,采用克隆形成实验检测不同浓度PPⅥ[0(对照组)、2、4、8 μmol/L]作用14 d后的细胞克隆数和克隆形成率,采用流式细胞术和Western blot法分别检测不同浓度PPⅥ[0(对照组)、4、8 μmol/L]作用24 h后的细胞凋亡率和凋亡相关蛋白[B细胞淋巴瘤2(Bcl-2)、Bcl-2相关X蛋白(Bax)、切割的胱天蛋白酶3(cleaved caspase-3)]、Fas/Fas配体(FasL)死亡受体通路相关蛋白、蛋白激酶B(又称Akt)/糖原合成激酶3β(GSK-3β)通路相关蛋白的表达情况.结果 与对照组比较,PPⅥ各浓度组细胞的存活率、克隆数和克隆形成率、Bcl-2蛋白的表达水平和Akt、GSK-3β蛋白的磷酸化水平均显著降低(P＜0.05或P＜0.01);细胞凋亡率,Bax、cleaved caspase-3蛋白和Fas、FasL、cleaved caspase-8蛋白的表达水平均显著升高(P＜0.05或P＜0.01).结论 PPⅥ可抑制人胶质瘤LN229细胞的增殖并诱导其凋亡,这种作用可能与激活Fas/FasL死亡受体通路和抑制Akt/GSK-3β通路有关.

Paris polyphylla var. yunnanensis (Franch.) Hand.-Mazz. (Melanthiaceae), an important specie of the genus Paris, has long been in a traditional Chinese medicine (TCM) for a long time. This study aimed to isolate and identify the structures of bioactive saponins from the rhizomes of P. polyphylla var. yunnanensis and evaluate their cytotoxicity against BxPC-3, HepG2, U373 and SGC-7901 carcinoma cell lines. Seven previously undescribed and seven known saponins were identified, and Paris saponins VII (PSVII) showed significant cytotoxicity against the BxPC-3 cell line with IC50 values of 3.59 μM. Furthermore, flow cytometry, transmission electron microscopy and western-bolt analysis revealed that PSVII inhibited the proliferation of BxPC-3 cells and might be involved in inducing apoptosis and pyroptosis by activating caspase-3, -7 and caspase-1, respectively.

The chemical constituent investigation on the root bark of Ailanthus altissima leads to the isolation of a new β-carboline alkaloid, 14(S),15-dihydroxy-6-methoxy-β-carboline (1), along with nine known alkaloids. The structure of new compound was elucidated on basis of extensive spectroscopic analysis, especially two-dimensional (2D) NMR techniques and the absolute configuration of C-14 was determined by ECD calculation. The neuroprotective effect of the isolated compounds on PC12 cells against the serum deprivation injury was evaluated by MTT method. As a result, compound 7 revealed protective effect on PC12 cells and the cell survival rate was significantly increased.