White crystalline powder
Buxus sinica (Rehd. et Wils.) Cheng subsp. sinica var. parvifolia M. Cheng
9,19-Cyclopregnan-16-ol, 4,4,14-trimethyl-3,20-bis(methylamino)-, (3β,5α,9β,16α,20S)-/bebuxine/cyclovirobuxind/cyclovirobuxinum D/cyclobuxine D/(3β,5α,9β,16α,20S)-4,4,14-Trimethyl-3,20-bis(methylamino)-9,19-cyclopregnan-16-ol/cvb-d/Cyclovirobuxine-D/CYCLOVIROBUXINE
495.7±10.0 °C at 760 mmHg
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For Reference Standard and R&D, Not for Human Use Directly.
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The blood-brain barrier (BBB) restricts the delivery of most drugs to the brain. In our previous study, the feasibility of cyclovirobuxine D delivery to the brain by a non-invasive nasal route was evaluated. In this study, a suitable drug delivery system by way of intranasal administration was developed, which could improve brain targeting. First, a formulation of cyclovirobuxine D (CVB-D) based on chitosan nanoparticles (CS-CVB-D-NPs) was prepared by the modified ionotropic gelation method through single-factor screening experiment. The CS-CVB-D-NPs with a entrapment efficiency (EE) of (62.82±2.59)% were found to be of a narrow polydispersity index (PI) (0.19±0.01) and (235.37± 12.71) nm in size, with a zeta potential of (33.9 ± 1.7) mV. The NPs possessed a sustained release characterization with in vitro release of 88.03 ± 2.30% at 24 h. In vivo, the higher AUC0-t(brain) of CS-CVB-D-NPs by intranasal administration revealed the development of a novel brain-targeting delivery method of CVB-D.
A Novel Delivery Method of Cyclovirobuxine D for Brain-Targeting: Chitosan Coated Nanoparticles Loading Cyclovirobuxine D by Intranasal Administration.
Wei H1, Lai S1, Wei J1, Yang L2, Jiang N1, Wang Q1, Yu Y1.
2018 Aug 1
The clinical application of doxorubicin (DOX) is compromised by its cardiac toxic effect. Cyclovirobuxine D (CVB-D) is a steroid alkaloid extracted from a traditional Chinese medicine, Buxus microphylla. Our results showed that CVB-D pretreatment markedly attenuated DOX-induced cardiac contractile dysfunction and histological alterations. By using TUNEL assay and western blot analysis, we found that CVB-D pretreatment reduced DOX-induced apoptosis of myocardial cells and mitochondrial cytochrome c release to cytosol. CVB-D pretreatment ameliorated DOX-induced cardiac oxidative damage including lipid peroxidation and protein carbonylation and a decrease in the ratio of reduced glutathione (GSH) to oxidized glutathione (GSSG). Moreover, CVB-D was found to prevent DOX-induced mitochondrial biogenesis impairment as evidenced by preservation of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and nuclear respiratory factor 1 (NRF1), as well as mitochondrial DNA copy number. These findings demonstrate that CVB-D protects against DOX-induced cardiomyopathy, at least in part, by suppression of oxidative damage and mitochondrial biogenesis impairment.
Cyclovirobuxine D Attenuates Doxorubicin-Induced Cardiomyopathy by Suppression of Oxidative Damage and Mitochondrial Biogenesis Impairment.
Guo Q1, Guo J2, Yang R2, Peng H2, Zhao J2, Li L3, Peng S2.
Gliomas are the most common neoplasm of the human central nervous system. Glioblastoma multiforme (GBM) is one of the most serious types of gliomas. Although considerable progress has been made in the development of cancer therapeutic agents, several antineoplastic drugs fail to penetrate the blood?brain barrier (BBB), resulting in a low survival rate of glioma patients. Recent studies have revealed that the traditional Chinese medicine Buxus microphylla contains the main active component Cyclovirobuxine D (CVB?D), which can cross the BBB with a novel delivery system. However, it remains unclear whether CVB?D exerts anticancer effects against GBM and low?grade glioma (LGG). The aim of the present study was to explore the feasibility of CVB?D as a new effective agent in the treatment of GBM and LGG. The ability of CVB?D to inhibit GBM and LGG cell proliferation was detected by CCK8 assay. Flow cytometry was used to detect cell cycle progression and apoptosis induction by Annexin V?FITC/PI assay. The expression levels of the apoptosis?associated proteins, namely cleaved caspase?3 and Bax/Bcl?2, were detected by western blot analysis. The mitochondrial membrane potential (ΔΨm) was detected by Rh123 dyed fluorescence micrograph. Hoechst staining was used to observe the morphological characteristics of the apoptotic cells. The scratch test was used to evaluate the migration of GBM and LGG cells. The results indicated that CVB?D reduced cell viability of T98G and Hs683 cells. Flow cytometry demonstrated that CVB?D?treated cells were arrested at the S phase of their cell cycle. The expression levels of the apoptosis?associated proteins were increased in CVB?D?treated cells. Rh123 and Hoechst staining indicated morphological changes and mitochondrial membrane potential changes of the cells undergoing apoptosis. The data confirmed that CVB?D inhibited cell proliferation by arresting the cell cycle of GBM and LLG cells and that it promoted the induction of cell apoptosis by altering the mitochondrial membrane potential. The findings of the present study indicate the potential value of CVB?D in the treatment of glioma.
Cyclovirobuxine D inhibits cell proliferation and migration and induces apoptosis in human glioblastoma multiforme and low?grade glioma.
Zhou L1, Tang H2, Wang F3, Ou S1, Wu T1, Fang Y1, Xu J1, Guo K1.