herb of Rabdosia rubescens (Hamst.) C.Y.Wu et Hsuan
ORIDONIN/Rubescensin/ISODONAL/(1α,5β,6β,7β,8α,9β,10α,13α,14R)-1,6,7,14-Tetrahydroxy-7,20-epoxykaur-16-en-15-one/RUBESCENSIN A/7a,20-Epoxy-1a,6b,7,14-tetrahydroxy-Kaur-16-en-15-one Isodonol/Isodonol/megathyrin A/Rabdosia rubescens
Methanol; Acetontrile; DMSO
599.8±50.0 °C at 760 mmHg
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Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:28957-04-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
To investigate the influence of oridonin on the killing activity of NK-92 MI cells targeting THP1 and the related mechanism.
The killing activity of NK-92 MI to THP1 before and after oridonin treatment was detected by LDH release assay; the expression of natural killer cell ligands activating receptor D (NKG2D, including MICA, MICB, ULBP1, ULBP2 and ULBP3) was detected by real-time quantitative polymerase chain reaction (qRT-PCR) and Western blot respectively; the expression of cytokine TNF-α, TNF-β and IFN-γ in the co-culture supernatant of NK-92 MI cells and THP1 cells were measured by ELISA.
The killing efficiency after oridonin treatment at different effector-target ratio (1:1, 5:1, 10:1) was all significantly up-regulated in comparison with that before oridonin treatment (P＜0.05). QRT-PCR and Western blot showed that the expressions of mRNA and protein levels of MICB, ULBP1, ULBP2 increased to varying degree (P＜0.05), but the expression levels of MICA and ULBP3 were not statistically significant between experimental group and control group (P＞0.05). ELISA results indicated that IFN-γ and TNF-β release were significantly increased after oridonin treatment (P＜0.05), however, the TNF-α release was not statistically different in comparison with control group (P＞0.05).
Oridonin can significantly improve killing efficiency of NK-92 MI on THP1, that might be related with up-regulation of MICB, ULBP1 and ULBP2 expression and promotion of IFN-γ and TNF-β release.
[Influence of Oridonin on the Icilling Acitivity of NK-92 MI Cells Targeting Cell THP1 and Its Mechanism].
Liu YF1, Jia Y2, He PC3, Zhang M3, He Q4.
Oridonin (ORI) is a natural active ingredient with strong anticancer activity. But its clinical use is restricted due to its poor water solubility, short half-life, and low bioavailability. The aim of this study is to utilize the metal organic framework material MOF-5 to load ORI in order to improve its release characteristics and bioavailability. Herein, MOF-5 was synthesized by the solvothermal method and direct addition method, and characterized by Scanning Electron Microscopy (SEM), X-Ray Diffraction (XRD), Fourier Transform Infrared Spectrometer (FTIR), Thermogravimetric Analysis (TG), Brunauer-Emmett-Teller (BET), and Dynamic Light Scattering (DLS), respectively. MOF-5 prepared by the optimal synthesis method was selected for drug-loading and in vitro release experiments. HepG2 cells were model cells. MTT assay, 4′,6-diamidino-2-phenylindole (DAPI) staining and Annexin V/PI assay were used to detect the biological safety of blank carriers and the anticancer activity of drug-loaded materials. The results showed that nano-MOF-5 prepared by the direct addition method had complete structure, uniform size and good biocompatibility, and was suitable as an ORI carrier. The drug loading of ORI@MOF-5 was 52.86% ± 0.59%. The sustained release effect was reliable, and the cumulative release rate was about 87% in 60 h. ORI@MOF-5 had significant cytotoxicity (IC50:22.99 μg/mL) and apoptosis effect on HepG2 cells. ORI@MOF-5 is hopeful to become a new anticancer sustained release preparation. MOF-5 has significant potential as a drug carrier material.
Antitumor; HepG2 cells; MOF-5; Oridonin; sustained release
Investigation of Metal-Organic Framework-5 (MOF-5) as an Antitumor Drug Oridonin Sustained Release Carrier.
Chen G1, Luo J2, Cai M3, Qin L4, Wang Y5, Gao L6, Huang P7, Yu Y8, Ding Y9, Dong X10, Yin X11, Ni J12,13.
2019 Sep 16
Oridonin (ORI) is a natural diterpenoid presented in some medicinal plants. The effects of pre-treatments from ORI against MPP+- or kainic acid (KA)-induced damage in nerve growth factor (NGF)-differentiated PC12 cells were investigated. Results showed that pre-treatments of ORI at 0.25-2 μM enhanced the viability and plasma membrane integrity of NGF-differentiated PC12 cells. MPP+ or KA exposure down-regulated Bcl-2 mRNA expression, up-regulated Bax mRNA expression, increased caspase-3 activity and decreased Na+-K+ ATPase activity. ORI pre-treatments at test concentrations reversed these changes. ORI pre-treatments decreased reactive oxygen species production, raised glutathione level, and increased glutathione peroxidase, glutathione reductase and catalase activities in MPP+ or KA treated cells. ORI pre-treatments lowered tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6 and prostaglandin E2 levels in MPP+ or KA treated cells. ORI also diminished MPP+ or KA induced increase in nuclear factor-κB binding activity. MPP+ exposure suppressed tyrosine hydroxylase (TH) mRNA expression and decreased dopamine content. KA exposure reduced glutamine synthetase (GS) mRNA expression, raised glutamate level and lowered glutamine level. ORI pre-treatments at 0.5-2 μM up-regulated mRNA expression of TH and GS, restored DA and glutamine content. These findings suggested that oridonin was a potent neuro-protective agent against Parkinson’s disease and seizure.
Copyright © 2019 Elsevier Ltd. All rights reserved.
NGF-differentiated PC12 cells; Oridonin; Parkinson's disease; Seizure
Oridonin, A natural diterpenoid, protected NGF-differentiated PC12 cells against MPP+- and kainic acid-induced injury.
Lin KH1, Li CY2, Hsu YM3, Tsai CH4, Tsai FJ5, Tang CH6, Yang JS7, Wang ZH8, Yin MC9.
Oridonin, a diterpenoid isolated from Rabdosia rubescens, acts as an inhibitor of AKT, with IC50s of 8.4 and 8.9 μM for AKT1 and AKT2; Oridonin possesses anti-tumor, anti-bacterial and anti-inflammatory effects.