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Tubeimoside I

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-T3014

  • Specification : 98%

  • CAS number : 102040-03-9

  • Formula : C63H98O29

  • Molecular Weight : 1319.43

  • PUBCHEM ID : 5462420

  • Volume : 25mg

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Catalogue Number

BF-T3014

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

1319.43

Appearance

White crystalline powder

Botanical Source

Bolbostemma paniculatum

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

Synonyms

TUBEIMOSIDE 1/β-D-Xylopyranosyl-(1->3)-6-deoxy-α-L-mannopyranosyl-(1->2)-1-O-{[(2R,3S,4S,4aR,5aS,8S,9S,9aR,17aR,17bR,19aR,19bS,21aS,25aS,27aR,27bR,29S,29aR,30aR)-3,4,8,9,13,29-hexahydroxy-2-(hydroxymethyl)-1 3,17a,19a,19b,24,24,27b-heptamethyl-11,15-dioxo-3,4,4a,7,8,9,9a,12,13,14,15,17a,18,19,19a,19b,20,21,22,23,24,25,25a,27,27a,27b,28,29,29a,30a-triacontahydro-2H,5aH,11H,17H-piceno[3,4-h]dipyrano[3,2-b:3 ;',2'-e][1,4,7,11]tetraoxacyclohexadecin-21a(/TubeimosideI/TUBELMOSIDEA/TUBEMOSIDE A/TUBEIMOSIDE I (RG)/(1S,4S,7S,8S,9R,11S,13S,14S,18S,22S,25S,27R,28S,29S,30R,32R,34R,35S,37R,38R,41R,42R,46S,53S,54R,55R,56R,57S,58R)-7,8,18,28,29,35,55,56,58-Nonahydroxy-30,54-bis(hydroxymethyl)-13,18,37,41,48,48,53,54-o ;ctamethyl-2,16,20-trioxo-3,5,10,12,15,21,24,26,31,33-decaoxadecacyclo[39.9.3.2.2.1.0.0.0.0.0]octapentacont-44-en-57-yl β-D-xylopyranosideOlean-12-en-28-oicacid,3-[[2-O-[4-O-(4-carboxy-3/α-L-Arabinopyranose, O-β-D-xylopyranosyl-(1->3)-O-6-deoxy-α-L-mannopyranosyl-(1->2)-1-O-[[(2R,3S,4S,4aR,5aS,8S,9S,9aR,17aR,17bR,19aR,19bS,21aS,25aS,27aR,27bR,29S,29aR,30aR)-3,4,4a,5a,8,9,9a ,12,13,14,15,17a,18,19,19a,19b,20,21,22,23,24,25,25a,27,27a,27b,28,29,29a,30a-triacontahydro-3,4,8,9,13,29-hexahydroxy-2-(hydroxymethyl)-13,17a,19a,19b,24,24,27b-heptamethyl-11,15-dioxo-2H,7H,11H,17H- piceno[3,4-h]dipyrano[3,2-b:3',2'-e][1,4,7,1/Lobatoside H/Tubeimoside I

IUPAC Name

Density

1.5±0.1 g/cm3

Solubility

Methanol; Water

Flash Point

Boiling Point

Melting Point

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2933390000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:102040-03-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30065205

Abstract

Parkinson’s disease (PD), a frequent degenerative disease in the elderly, is characterized by dopaminergic neurodegeneration in the substantia nigra pars compacta (SNpc). Neuroinflammation caused by over-activated microglia plays a crucial role in the pathogenesis of PD. Tubeimoside I (TBMS1) has a broad anti-inflammatory effect in peripheral tissues, but the effect on neuroinflammation has not been reported. Therefore, we explored whether TBMS1 could protect dopaminergic neurons by inhibiting the activation of microglia in lipopolysaccharide (LPS)-induced PD rat model. In addition, then, the effect and mechanism of TBMS1 on neuroinflammation were assessed in LPS-exposed murine microglial BV-2 cells. The results in vivo showed that TBMS1 suppressed microglial activation and dopaminergic neurons’ reduction in LPS-injected PD rat model. In vitro study found that TBMS1 could inhibit LPS-induced inflammatory responses in BV-2 cells, and this effect was mediated by suppressing the phosphorylation of protein kinase B (AKT), nuclear factor-kappa B (NF-κB p65), p38 and extracellular regulated protein kinases (ERK1/2). Taken together, these results demonstrated for the first time that TBMS1 played a role in protecting dopaminergic neurons by inhibiting neuroinflammation mediated by microglia.

KEYWORDS

MAPKs; NF-κB; Parkinson’s disease; Tubeimoside I; microglia.

Title

Tubeimoside I Protects Dopaminergic Neurons Against Inflammation-Mediated Damage in Lipopolysaccharide (LPS)-Evoked Model of Parkinson's Disease in Rats

Author

Dewei He 1 , Bingxu Huang 2 , Shoupeng Fu 3 , Yuhang Li 4 , Xin Ran 5 , Yandan Liu 6 , Guangxin Chen 7 , Juxiong Liu 8 , Dianfeng Liu 9

Publish date

2018 Jul 31

PMID

29434745

Abstract

In the present study, the effects of tubeimoside I (TBMS1) on particulate matter <2.5 µm in diameter (PM2.5)-induced pulmonary injury and its mechanisms of action were investigated. Male BALB/c mice were randomly assigned into five groups (n=10/group): Control, PM2.5, PM2.5 + TBMS1 45 mg/kg, PM2.5 + TBMS1 90 mg/kg and PM2.5 + TBMS1 180 mg/kg. The dose of the PM2.5 suspension administered to the mice was 40 mg/kg via nasal instillation. The PM2.5 + TBMS1 groups received TBMS1 daily orally for 21 consecutive days, while the mice in the control and PM2.5 groups received equivalent volumes of PBS. Subsequently, lactic dehydrogenase, acid phosphatase, alkaline phosphatase, albumin, tumor necrosis factor-α and interleukin-6 protein levels in bronchoalveolar lavage fluid were determined. Oxidative stress was evaluated by detecting the protein levels of malondialdehyde, superoxide dismutase and inducible nitric oxide synthase, and the level of nitric oxide in lung tissue. Lastly, histopathological images of lung sections were obtained to observe changes in the lung tissue with treatment. The results indicated that exposure to PM2.5 induced pathological pulmonary changes, and biofilm and parenchymal cell damage, and promoted inflammation and oxidative stress. Treatment with TBMS1 attenuated the development of PM2.5-induced pulmonary injury. Its mechanisms of action were associated with reducing cytotoxic effects, levels of inflammatory mediators and oxidative damage. In conclusion, the results of the present study indicate that TBMS1 is a potential therapeutic drug for treating PM2.5-induced pulmonary injury.

KEYWORDS

inflammation; oxidative damage; particle matter <2.5 µm in diameter; pulmonary injury; tubeimoside I.

Title

Tubeimoside I Attenuates Inflammation and Oxidative Damage in a Mice Model of PM 2.5-induced Pulmonary Injury

Author

Jin-Bo Zhang 1 , Lei Zhang 2 , Shi-Qing Li 3 , Ai-Hua Hou 4 , Wei-Chao Liu 1 , Ling-Ling Dai 4

Publish date

2018 Feb

PMID

30389907

Abstract

Cervical cancer is one of the most aggressive human cancers with poor prognosis due to constant chemoresistance and repeated relapse. Tubeimoside I (TBM) has been identified as a potent antitumor agent that inhibits cancer cell proliferation by triggering apoptosis and inducing cell cycle arrest. Nevertheless, the detailed mechanism remains unclear and needs to be further elucidated, especially in cervical cancer. In this study, we found that TBM could induce proliferation inhibition and cell death in cervical cancer cells both in vitro and in vivo. Further results demonstrated that treatment with TBM could induce autophagosome accumulation, which was important to TBM against cervical cancer cells. Mechanism studies showed that TBM increased autophagosome by two pathways: First, TBM could initiate autophagy by activating AMPK that would lead to stabilization of the Beclin1-Vps34 complex via dissociating Bcl-2 from Beclin1; Second, TBM could impair lysosomal cathepsin activity and block autophagic flux, leading to accumulation of impaired autophagolysosomes. In line with this, inhibition of autophagy initiation attenuated TBM-induced cell death, whereas autophagic flux inhibition could exacerbated the cytotoxic activity of TBM in cervical cancer cells. Strikingly, as a novel lethal impaired autophagolysosome inducer, TBM might enhance the therapeutic effects of chemotherapeutic drugs towards cervical cancer, such as cisplatin and paclitaxel. Together, our study provides new insights into the molecular mechanisms of TBM in the antitumor therapy, and establishes potential applications of TBM for cervical cancer treatment in clinic.

Title

Tubeimoside I Induces Accumulation of Impaired Autophagolysosome Against Cervical Cancer Cells by Both Initiating Autophagy and Inhibiting Lysosomal Function

Author

Xuping Feng 1 2 , Jing Zhou 2 , Jingyi Li 3 , Xueyan Hou 4 , Longhao Li 1 5 , Yongmin Chen 6 , Shuyue Fu 2 , Li Zhou 2 , Changlong Li 7 , Yunlong Lei 8

Publish date

2018 Nov 2


Description :

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].