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Solasodine

$225

  • Brand : BIOFRON

  • Catalogue Number : BF-S3026

  • Specification : 98%

  • CAS number : 126-17-0

  • Formula : C27H43NO2

  • Molecular Weight : 413.64

  • PUBCHEM ID : 442985

  • Volume : 25mg

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Catalogue Number

BF-S3026

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

413.64

Appearance

White crystalline powder

Botanical Source

Solanum nigrum

Structure Type

Alkaloids

Category

Standards;Natural Pytochemical;API

SMILES

CC1CCC2(C(C3C(O2)CC4C3(CCC5C4CC=C6C5(CCC(C6)O)C)C)C)NC1

Synonyms

(3b,22a,25R)-Spirosol-5-en-3-ol/Solanearpidine/Solasod-5-en-3β-ol/(3β,22α,25R)-Spirosol-5-en-3-ol/Solancarpidine/Solasod-5-en-3b-ol/Solasod-5-en-3β-ol (8CI)/Purapuridine/Solasod-5-en-3-β-ol/Solanidine-S/Solasodine/Spirosol-5-en-3-ol, (3β,22α,25R)-/D5-20bF,22aF,25aF,28-azaspirosten-3b-ol

IUPAC Name

(1S,2S,4S,5'R,6R,7S,8R,9S,12S,13R,16S)-5',7,9,13-tetramethylspiro[5-oxapentacyclo[10.8.0.02,9.04,8.013,18]icos-18-ene-6,2'-piperidine]-16-ol

Applications

Solasodine(Purapuridine) is a poisonous alkaloid chemical compound that occurs in plants of the Solanaceae family. Solasodine showed selective cytotoxicity against cervical cancer cell line (HeLa) and human myeloid leukemia cell line (U937).IC50 Value: 12.17 ± 3.3 uM (Hela cell line)[1]Target: Anticancerin vitro: Mouse embryonic teratocarcinoma P19 cells exposed to solasodine for 2 days followed by a 5-day washout differentiated into cholinergic neurons that expressed specific neuronal markers and displayed important axonal formation that continued growing even 30 days after treatment [2].in vivo: A 2-week infusion ofsolasodine into the left ventricle of the rat brain followed by a 3-week washout resulted in a significant increase in bromodeoxyuridine uptake by cells of the ependymal layer, subventricular zone, and cortex that co-localized with doublecortin immunostaining, demonstrating the proliferative and differentiating properties of solasodine on neuronal progenitors. Solasodine treatment in rats resulted in a dramatic increase in expression of the cholesterol- and drug-binding translocator protein in ependymal cells, suggesting a possible role played by neurosteroid production in solasodine-induced neurogenesis. In GAD65-GFP mice that express the green fluorescent protein under the control of the glutamic acid decarboxylase 65-kDa promoter, solasodine treatment increased the number of GABAergic progenitors and neuroblasts generated in the subventricular zone and present in the olfactory migratory tract [2]. intraperitoneal (i.p.) injection of solasodine (25 mg/kg) significantly delayed (p < 0.01) latency of hind limb tonic extensor (HLTE) phase in the PCT-induced convulsions. In the MES model, solasodine significantly reduced (p < 0.001) duration of HLTE at 25, 50, and 100 mg/kg, i.p. in a dose-dependent manner [3]. Oral administration (80 mg/kg body wt/day for 30 days) of solasodine (extracted and isolated from the berries of the Solanum xanthocarpum) to intact dogs significantly decreased the epithelial cell height of cauda epididymides [4].

Density

1.1±0.1 g/cm3

Solubility

Methanol; Chloroform

Flash Point

279.1±30.1 °C

Boiling Point

537.9±50.0 °C at 760 mmHg

Melting Point

284 °C (dec.)(lit.)

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2906190000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:126-17-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

28283413

Abstract

Solasodine, a naturally occurring aglycone of glycoalkaloid in eggplant (Solanum melongena), was found to inhibit proliferation in various tumor cells. However, the effect of solasodine on cancer cell metastasis remains unclear. This study investigates the suppression mechanism of solasodine on motility of human lung cancer cell A549 in vitro. Results show that solasodine reduces viability of A549 cells. Treatment with non-toxic doses of solasodine suppresses markedly cell invasion. Solasodine reduces the mRNA level of matrix metalloproteinase-2 (MMP-2), MMP-9 and extracellular inducer of matrix metalloproteinase (EMMPRIN), but increases the expression of reversion-inducing cysteine-rich protein with kazal motifs (RECK), as well as tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIMP-2. Immunoblotting assays indicate that solasodine is effective in suppressing PI3K and Akt phosphorylation. Moreover, solasodine downregulates oncogenic microRNA-21 (miR-21), which has been known to target RECK. Downregulation of miR-21 by miR-21 inhibitor increases RECK expression and decreases cell invasion, suggesting that downregulation of miR-21 by solasodine may contribute to elevate RECK expression and subsequently inhibiting cell invasion. Taken together, the results reveal that inhibition of A549 cell invasion by solasodine may be, at least in part, through blocking MMP expression. Solasodine also reduces PI3K/Akt signaling pathways and downregulates expression of miR-21. These findings demonstrate an attractive therapeutic potential for solasodine in lung cancer anti-metastatic therapy.

KEYWORDS

Cell invasion; Lung cancer; Matrix metalloproteinase; MicroRNA-21; Solasodine

Title

Solasodine Inhibits Invasion of Human Lung Cancer Cell Through Downregulation of miR-21 and MMPs Expression

Author

Kun-Hung Shen 1 , Jui-Hsiang Hung 2 , Chia-Wei Chang 2 , Yu-Ting Weng 2 , Ming-Jiuan Wu 2 , Pin-Shern Chen 3

Publish date

2017 Apr 25

PMID

30268504

Abstract

Adverse side effects of conventional chemotherapy, acquired resistance and fatal tumor metastasis of human colorectal cancer (CRC) are propelling the exploration for novel selective anticarcinogens. Solasodine is a main active component isolated from Solanum incanum L that exhibited a potent stemness and invasion inhibitory effect on human colorectal cancer HCT116 cells. Colony Spheroid formation assay showed that solasodine dose-dependently prohibited HCT116 cell stemness. CD133, CD44, Nanog, Oct-4 and Sox-2 were inhibited by solasodine to reverse stemness and similar mechanism was stimulated in vivo. Transwell and scratch wound assays revealed that solasodine impeded HCT116 cell invasion and migration potential strengthened by TGF-β1. Moreover, solasodine attenuated TGF-β1-induced EMT and decreased MMPs while in vivo study showed the same trend. The results of this study implied that solasodine may be a novel therapeutic drug for CRC treatment.

KEYWORDS

Colorectal cancer; Epithelial-mesenchymal transition; Migration; Solasodine; Stemness.

Title

Solasodine Reverses Stemness and Epithelial-Mesenchymal Transition in Human Colorectal Cancer

Author

Yu-Wen Zhuang 1 , Cun-En Wu 2 , Jin-Yong Zhou 2 , Zhi-Ming Zhao 3 , Chun-Li Liu 3 , Jun-Yi Shen 3 , Hui Cai 4 , Shen-Lin Liu 5

Publish date

2018 Oct 28

PMID

27462871

Abstract

Solasodine, a steroidal alkaloid isolated from solanaceous species, exhibits anticancer activities on several cell lines. This study aimed to explore the antitumor potential of solasodine on ovarian cancer cells. The MTT assay, lactate dehydrogenase release assay, Hoechst 33342 staining, 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethyl-imidacarbocyanine staining assay, and Annexin V/PI assay were conducted to investigate the antiproliferation and apoptosis-inducing effects of solasodine. Monodansylcadaverine staining was performed to label the acidic puncta on ovarian cancer HEY cells. A wound healing assay and Transwell assay were carried out to determine whether solasodine elicits an antimetastatic effect on HEY cells. A gelatin zymography assay was applied to detect the enzymatic activities of matrix metalloproteinases. Western blot was employed to examine relevant protein expression. Results revealed that solasodine inhibited cell viabilities in a time- and dose-dependent manner, triggered apoptotic body formation, reduced cell mitochondrial membrane potential, and interfered with autolysosome degradation in ovarian cancer cells. Solasodine also suppressed the migration and invasion of HEY cells by downregulating matrix metalloproteinase expression and activities. This study could be used as a basis for further studies on the molecular mechanisms of the antiproliferation, apoptosis-inducing, autophagy-modifying, and antimetastatic activities of solasodine.

Title

Solasodine Induces Apoptosis, Affects Autophagy, and Attenuates Metastasis in Ovarian Cancer Cells

Author

Xiao-Huang Xu 1 , Le-Le Zhang 1 , Guo-Sheng Wu 2 , Xin Chen 1 , Ting Li 1 , Xiuping Chen 1 , Yi-Tao Wang 1 , Jin-Jian Lu 1

Publish date

2017 Feb