Rubusoside is a natural sweetener and a solubilizing agent with antiangiogenic and antiallergic properties. Rubusoside is an excellent solubilizing agent. It can enhance the solubility of a number of pharmaceutically important compounds, such as liquiritin, teniposide, curcumin, and etoposide.
Catalpol, an iridoid glycoside, has neuroprotective, anti-inflammatory, and anti-hepatitis virus effects.IC50 Value:Target: neuroprotective, anti-inflammatory, and anti-hepatitis virus natural product.In vitro: Catalpol could be encapsulated into composite nanofibers and induce differentiation of hASCs into neural-like cells, which might offer new avenues in nerve regeneration [1].In vivo: The pharmacokinetics of catalpol in normal and doxorubicin-induced chronic kidney disease rats after oral administration of Rehmannia glutinosa extract was determined, and the extraction recoverie of catalpol was higher than 68.24% [2]. The protective effect of catalpol on renal IRI mice through suppressing phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt)-endothelial nitric oxide synthase (eNOS) and against inflammation, and the possible underlying mechanism [3].
Ganoderic acid can Inhibitt of the JAK-STAT3 signaling pathway, also inhibit proliferation, viability, ROS.In vitro: A lower doses of Ganoderic acid enhance HLA class II-mediated antigen presentation and CD4+ T cell recognition of lymphoma. [1] ganoderic acid A promots cisplatin-induced cell death by enhancing the sensitivity of HepG2 cells to cisplatin mainly via the signal transducer and activator of transcription 3 suppression. [2] Ganoderic acid A inhibits proliferation, viability, ROS, DPPH, and analyzed the expression of SOD1, SOD2, and SOD3 by Real time PCR in a PC-3 cell in a dose-dependent manner.[3] GA-A effectively inhibites the proliferation of human osteosarcoma HOS and MG-63 cells in a dose-dependent manner, and induced obvious cell apoptosis in both cells.[4]In vivo: Ganoderic acid -treatment significantly prolonged survival of EL4 challenged mice and decreased tumor metastasis to the liver.[1]
Rosmarinic acid (RA) is a widespread phenolic ester compound in the plants. Rosmarinic acid inhibits MAO-A, MAO-B and COMT enzymes with IC50s of 50.1, 184.6 and 26.7 μM, respectively.
Lathyrol is a natural product, and is used for cancer treatment.
Eleutheroside E, a principal component of Eleutherococcus enticosus, has anti-inflammatory and protective effects in ischemia heart. IC50 value:Target:In vitro: Treatment of 10 μM Eleutheroside E (EE) for 24 h increased basal glucose uptake as well as improved TNF-α-mediated suppression of glucose uptake. [2]In vivo: To investigate the effect of Eleutheroside E (EE) on arthritis, the CIA model in DBA/1 mice was used. Compared to vehicle-treated CIA mice, 15 mg/kg TG treatment and 30 and 60 mg/kg EE treatment obviously decreased the arthritis scores and body weight loss in CIA mice (P<0.01) [1].
Aucubin is an iridoid glycoside with a wide range of biological activities, including anti-inflammatory, anti-microbial, anti-algesic as well as anti-tumor activities.IC50 value:Target:In vitro: Aucubin promotes neuronal differentiation and neurite outgrowth in neural stem cells cultured primarily from the rat embryonic hippocampus [1]. Aucubin significantly reversed the elevated gene and protein expression of MMP-3, MMP-9, MMP-13, iNOS, COX-2 and the production of NO induced by IL-1β challenge in rat chondrocytes [2]. In vivo:
Hederacoside D is one of the bioactive saponins from Hedera helix, and plays pivotal roles in the overall biological activity.
Betulin (Trochol), is a sterol regulatory element-binding protein (SREBP) inhibitor with an IC50 of 14.5 μM in K562 cell line.
Geniposidic acid is an effective anticancer and radioprotection agent.Target: OthersMice were given an intraperitoneal injection of Geniposidic acid (GA) (12.5, 25, 50 mg/kg) 1 h before receiving GA against d-galactosamine (GalN) (800 mg/kg)/LPS (40 μg/kg). Liver and blood samples were collected 1 and 8 h after GalN/LPS injection. The survival rate of the GA group was significantly higher than the control. GalN/LPS increased serum aminotransferase activity, serum tumor necrosis factor-α level and hepatic lipid peroxidation and decreased hepatic glutathione content [1]. GA enhanced significantly the postirradiation responses of splenic blastogenesis by PHA. In addition, GA is a potent tumor growth inhibitor when combined with the X-irradiation, though there was no significant synergetic effect on their combined antitumor activity. The preliminary results of GA on hematological and blastogenic observations in this study suggested that it may very well, partially, play a role in an effective anticancer product with the ability to decrease undesirable radiation damage to the hematologic tissue after high dose irradiation [2].
Dehydroandrographolide is extracted from herbal medicine Andrographis paniculata (Burm f) Nees; alleviate oxidative stress in LPS-induced acute lung injury possibly by inactivating iNOS.
Tubeimoside I(Lobatoside-H) is an extract from Chinese herbal medicine Bolbostemma paniculatum (MAXIM.) FRANQUET (Cucurbitaceae) has been shown as a potent anti-tumor agent for a variety of human cancers.IC50 value:Target: Anticancer natural compoundin vitro: TBMS I inhibited the proliferation of both HepG2 and L-02 cells in a dose- and time-dependent manner, but HepG2 cells appeared more sensitive to the agent. When exposed to TBMS I for 24, 48 and 72 h, IC50 for HepG2 cells versus L-02 cells were 15.5 vs. 23.1, 11.7 vs. 16.2, 9.2 vs. 13.1 (μM, p<0.01), respectively. TBMS I induced cell shrinkage, nuclear condensation and fragmentation, cell cycle arrest at the G2/M phase, mitochondrial membrane disruption, release of cytochrome c from the mitochondria, activation of caspase 3 and 9, and shifting Bax/Bcl-2 ratio from being anti-apoptotic to pro-apoptotic, all indicative of initiation and progression of apoptosis involving mitochondrial dysfunction [1]. TBMS1-induced molecular events were related to mitochondria-induced intrinsic apoptosis and P21-cyclin B1/cdc2 complex-related G2/M cell cycle arrest [2]. TBMS1 combined with CDDP promoted cell apoptosis, decreased proliferation activity and increased cytosolic Ca2+ levels. Bcl-2 protein expression was down-regulated but Bax was up-regulated. Moreover, GST-π mRNA and protein expression were decreased. TBMS1 reduced the resistance of the cells to CDDP-induced cytotoxicity [4]. Treatment with TBMS1 resulted in dose- and time-dependent inhibition of proliferation, led to arrest in phase G2/M of the cell cycle and increased the levels of intracellular Ca2?. Furthermore, TBMS1 up-regulated the levels of the glucose-regulated protein 78/immunoglobuin heavy chain binding protein (GRP78/Bip), C/EBP homologous protein (CHOP), Bax, and cleaved caspase-3 and down-regulated the levels of Bcl-2 [5].in vivo: TBMS1 significantly inhibited the production of the pro-inflammatory cytokines, TNF-α, IL-6 and IL-1β in vitro and in vivo. Pretreatment with TBMS1 markedly attenuated the development of pulmonary edema, histological severities and inflammatory cells infiltration in mice with ALI [3].
Pseudoginsenoside-F11 (PF11), a component of Panax quinquefolium (American ginseng), has been demonstrated to antagonize the learning and memory deficits induced by scopolamine, morphine and methamphetamine in mice. IC50 value: Inhibition of diprenorphine binding with an IC50 of 6.1 μM Target:In vitro: Biochemical experiments revealed that PF11 could inhibit diprenorphine (DIP) binding with an IC50 of 6.1 μM and reduced the binding potency of morphine in Chinese hamster ovary (CHO)-μ cells [2].In vivo: One in vivo model of cisplatin-induced acute renal failure was performed. The results showed that pretreatment with Pseudoginsenoside F11 reduced cisplatin-elevated blood urea nitrogen and creatinine levels, as well as ameliorated the histophathological damage [1]. We tested the effects of Pseudoginsenoside F11 on morphine-induced development of behavioral sensitization and alterations in glutamate levels in the medial prefrontal cortex (mPFC) in freely moving mice by using in vivo microdialysis. As the results shown, Pseudoginsenoside F11 antagonized the development of behavioral sensitization and decrease of glutamate in the mPFC induced by morphine [3].
Dehydrocostus Lactone is a major sesquiterpene lactone isolated from the roots of Saussurea lappa.IC50 value:Target:In vitro: Dehydrocostus Lactone promoted apoptosis with increased activation of caspases 8, 9, 7, 3, enhanced PARP cleavage, decreased Bcl-xL expression and increased levels of Bax, Bak, Bok, Bik, Bmf, and t-Bid. We have demonstrated that Dehydrocostus Lactone inhibits cell growth and induce apoptosis in DU145 cells [1]. Dehydrocostus Lactone inhibits NF-kappaB activation by preventing TNF-alpha-induced degradation and phosphorylation of its inhibitory protein I-kappaB alpha in human leukemia HL-60 cells and that dehydrocostus lactone renders HL-60 cells susceptible to TNF-alpha-induced apoptosis by enhancing caspase-8 and caspase-3 activities [2]. Dehydrocostus Lactone inhibited the production of NO in lipopolysaccharide (LPS)-activated RAW 264.7 cells by suppressing inducible nitric oxide synthase enzyme expression.In vivo: Dehydrocostus Lactone decreased the TNF-alpha level in LPS-activated systems in vivo [3].
5,15-Diacetyl-3-benzoyllathyrol is one of the lathyrane diterpenoids, that has anti-cancer activity.
Isoastragaloside IV is a triterpene oligoglycoside isolated from Astragali Radix.
Squalene is an intermediate product in the synthesis of cholesterol, and shows several pharmacological properties such as hypolipidemic, hepatoprotective, cardioprotective, antioxidant, and antitoxicant activity.
Notoginsenoside Fe is a natural compound isolated from Panax japlcus var.
Notoginsenoside Ft1 is a saponin isolated from Panax notoginseng; stimulator of angiogenesis.IC50 value:Target: angiogenesis stimulatorin vitro: Ft1 increases translocalization of hypoxia-inducible factor-1α (HIF-1α) from cytoplasm to nuclei, where it binds to the vascular endothelial growth factor (VEGF) promoter, increasing the expression of VEGF mRNA and the subsequent secretion of the growth factor. Ft1 induces the activation of PI3K/AKT and Raf/MEK/ERK signaling pathways [1]. Among the saponins examined, Ft1 was the most potent procoagulant and induced dose-dependent platelet aggregation. Ft1 reduced plasma coagulation indexes, decreased tail bleeding time and increased thrombogenesis. Moreover, it potentiated ADP-induced platelet aggregation and increased cytosolic Ca(2+) accumulation, effects that were attenuated by clopidogrel. Ft1 binds to platelet P2Y12 receptors. The increase in intracellular Ca(2+) evoked by Ft1 in HEK293 cells overexpressing P2Y12 receptors could be blocked by ticagrelor [2]. Ft1 caused endothelium-dependent relaxations, which were abolished by l-NAME (inhibitor of nitric oxide synthases) and ODQ (inhibitor of soluble guanylyl cyclase). Ft1 increased the cGMP level in rat mesenteric arteries. GR and ER? were present in the endothelial layer and their antagonism by RU486 and PHTPP, respectively, inhibited Ft1-induced endothelium-dependent relaxations and phosphorylations of eNOS, Akt and ERK1/2 [3]. Ft1 showed the best inhibitory effect on cell proliferation of SH-SY5Y cells with IC50 of 45μM. Ft1 not only arrested the cell cycle at S, G2/M stages, but also promoted cell apoptosis. Ft1 up-regulated the protein expressions of cleaved caspase 3, phospho-p53, p21, and cyclin B1, but down-regulated that of Bcl-2. Moreover, Ft1 enhanced the phosphorylation of ERK1/2, JNK and p38 MAPK [4].in vivo: Ft1 promotes the formation of blood vessels in Matrigel plug and wound healing in mice [1].
Alisol B is a potentially novel therapeutic compound for bone disorders by targeting the differentiation of osteoclasts as well as their functions.IC50 Value:Target:In vitro: The in vitro cultured human renal tubular epithelial HK-2 cells were intervened with 5 ng/mL transforming growth factor-beta (TGF-beta), 0.1 micromol C3a, and 0.1 micromol C3a + 10 micromol alisol B, respectively. Exogenous C3a could induce renal tubular EMT. Alisol B was capable of suppressing C3a induced EMT [1]. Alisol-B strongly inhibited RANKL-induced osteoclast formation when added during the early stage of cultures, suggesting that alisol-B acts on osteoclast precursors to inhibit RANKL/RANK signaling. Among the RANK signaling pathways, alisol-B inhibited the phosphorylation of JNK, which are upregulated in response to RANKL in bone marrow macrophages, alisol-B also inhibited RANKL-induced expression of NFATc1 and c-Fos, which are key transcription factors for osteoclastogenesis. In addition, alisol-B suppressed the pit-forming activity and disrupted the actin ring formation of mature osteoclasts [2]. Alisol B induced calcium mobilization from internal stores, leading to autophagy through the activation of the CaMKK-AMPK-mammalian target of rapamycin pathway. Moreover, the disruption of calcium homeostasis induces endoplasmic reticulum stress and unfolded protein responses in alisol B-treated cells, leading to apoptotic cell death. Finally, by computational virtual docking analysis and biochemical assays, it was showed that the molecular target of alisol B is the sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase [3].In vivo:
Cycloastragenol, a natural tetracyclic triterpenoid, was first identified when screening Astragalus membranaceus extracts for active ingredients with antiaging properties. IC50 value:Target:In vitro: In the study of Cycloastragenolon the treatment of degenerative diseases, the result showed that first-pass intestinal metabolism of cycloastragenol might occur upon passage through the intestinal epithelium. Cycloastragenol underwent extensive metabolism in rat and human liver microsomes with only 17.4% and 8.2%, respectively, of the starting amount of Cycloastragenol remaining after 30 min of incubation [1]. The present study demonstrates that cycloastragenol stimulates telomerase activity and cell proliferation in human neonatal keratinocytes. In particular, cycloastragenol promotes scratch wound closure of human neonatal keratinocyte monolayers in vitro [3]. In vivo: Rats were treated with Cycloastragenol (40 mg·kg- 1·d- 1) for 7 days to induce hepatic microsomal enzyme. The result showed that compared with the control, cycloastragenol obviously activated CYP2E1, and remarkably inhibited CYP3A4 [2].
Ginsenoside Rb1, a main constituent of the root of Panax ginseng, inhibits Na+, K+-ATPase activity with an IC50 of 6.3±1.0 μM. Ginsenoside also inhibits IRAK-1 activation and phosphorylation of NF-κB p65 .
Neoandrographolide is a diterpenoid from the Andrographis paniculata (Acanthaceae).
7-xylosyltaxol(Taxol-7-xyloside) is a taxol (Paclitaxel) derivative; Paclitaxel binds to tubulin and inhibits the disassembly of microtubules.IC50 Value:Target: Microtubule/TubulinPaclitaxel is a compound extracted from the Pacific yew tree with antineoplastic activity. Paclitaxel also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein Bcl-2 (B-cell Leukemia 2). Paclitaxel inhibits DNA synthesis and stimulates the release of tumor necrosis factor-α. Paclitaxel induces apoptosis in murine mammary carcinoma MCA-4 and ovarian carcinoma OCA-1 tumors.
20(R)-Protopanaxatriol is a natural aglycone of ginsenosides Re, Rf, Rg1, Rg2 and Rh.
Nagilactone B, extracted from the root bark of Podocarpus nagi, is a liver X receptor (LXR) agonist.
Ingenol-5,20-acetonide is an intermediate from ingenol for synthesis of ingenoids; improved stability compared to ingenol.
Andrographolide is a NF-κB inhibitor, which inhibits NF-κB activation through covalent modification of a cysteine residue on p50 in endothelial cells without affecting IκBα degradation or p50/p65 nuclear translocation.
Ginsenoside Rf is a trace component of ginseng root. Ginsenoside Rf inhibits N-type Ca2+ channel.
Melittoside is a natural compound.