A focal adhesion kinase inhibitor 16-hydroxy-cleroda-3,13-dien-16,15-olide incorporated into enteric-coated nanoparticles for controlled anti-glioma drug delivery

Thiyagarajan, Varadharajan; Lin, Shi-Xiang; Lee, Chia‐Hung; Weng, Ching‐Feng

doi:10.1016/j.colsurfb.2016.01.038

Cited by 21 publications

(20 citation statements)

References 47 publications

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“…Several studies also found that modulation of autophagy sensitizes brain tumor cells to standard radiotherapy and chemotherapy-induced death (Kaza et al, 2012). HCD could be a potential inhibitor of FAK and potentially used for anti-tumorigenesis and anti-metastasis treatments in our previous reports (Thiyagarajan et al, 2013(Thiyagarajan et al, , 2016b. However, the effect of HCD in regulating the autophagy of brain tumor cell lines neuroblastoma N18 and glioma C6 is still unclear.…”

Section: Introductionmentioning

confidence: 90%

16-hydroxy-cleroda-3,13-dien-16,15-olide induced glioma cell autophagy via ROS generation and activation of p38 MAPK and ERK-1/2

Thiyagarajan

Sivalingam

Viswanadha

et al. 2016

Environmental Toxicology and Pharmacology

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Section: Introductionmentioning

confidence: 90%

16-hydroxy-cleroda-3,13-dien-16,15-olide induced glioma cell autophagy via ROS generation and activation of p38 MAPK and ERK-1/2

Thiyagarajan

Sivalingam

Viswanadha

et al. 2016

Environmental Toxicology and Pharmacology

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“…Moreover, the peak intensity of aliphatic stretch higher in HCD immobilized MSNs when compared to that of MSN-NH 2 , confirmed its successful immobilization [41] through strong attractions with the amine-modified MSN surfaces. The surface charge of surfactant-extracted MSNs ensued with a negative charge (−35 mV) due to the silanol groups in the framework [41], which upon post-modification the MSNs resulted in having a positive charge, demonstrating enormous amine groups attached to the framework. This improved the affinity between drug and carrier, and subsequently increased drug loading efficiency.…”

Section: Discussionmentioning

confidence: 80%

“…Furthermore, the degradation temperature of HCD (Figure 2b,b′) in MSNs shifted towards the right (pure HCD degraded at around 285 °C) showing that the immobilization ensued inside the pores rather than on the surface, by which the stability of the sensitive drug improved after immobilization. We observed significant changes in structural properties (final BET surface area, pore volume, and pore size) within each modification in the MSN nanoconjugates [41] measured using N 2 adsorption–desorption isotherm curves (Figure 3, Table 1). In a similar fashion, the pore volume of the respective samples was reduced after amine modification and HCD immobilization, respectively.…”

Section: Discussionmentioning

confidence: 99%

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Encapsulation of 16-Hydroxycleroda-3,13-Dine-16,15-Olide in Mesoporous Silica Nanoparticles as a Natural Dipeptidyl Peptidase-4 Inhibitor Potentiated Hypoglycemia in Diabetic Mice

et al. 2017

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Natural supplements comprise good efficacy with less adverse effects as against diabetic therapy, but their advancement as anti-diabetic agents is unsatisfactory with regard to the delivery system. Dipeptidyl peptidase-4 (DPP4)/CD26) can degrade glucagon-like pepetide-1 (GLP-1) which renders a decrease of blood glucose levels. 16-hydroxycleroda-3,13-dine-16,15-olide (HCD) extracted from Polyalthia longifolia, exhibits numerous medicinal potentials including hypoglycemic potential. On consideration of HCD application, the bioavailability is affected by low solubility. Extended experiments of anti-diabetic efficacy confirmed HCD biocompatible with mesoporous silica nanoparticles (MSNs) encapsulation resulted in a sustained release property in delivering HCD for the inhibition of DPP4 via the activity and protein levels of DPP4 analysis. In the enzymatic activity assay, MSN-HCD directly changed DPP4 activity. Moreover, MSN-HCD nanoparticles were treated with Caco-2 cells and the protein levels of DPP4 determined within the cells. The results revealed that MSN-HCD caused reduction of DPP4 activity in a time- and dose-dependent fashion. Orally administered MSN-HCD in diet-induced diabetic mice alleviated blood glucose via an oral glucose tolerance test. In addition, administration of MSN-HCD for five weeks revealed that the biochemical cues such as pyruvate transaminase (GPT), glutamate oxaloacetate transaminase (GOT), triglycerides (TG), cholesterol (CHO), and glycated hemoglobin (HbA1c) in mice were commendable as further confirmation of MSN-HCD efficacy and less adverse effects in down-regulation of hyperglycemia. Furthermore, this formulation effectively controlled blood glucose and significantly decreased the body weight of mice, suggesting that MSN-HCD exerts natural DPP4 inhibitor as a potential clinical drug for the treatment of diabetes.

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“…Recently, Thiyagarajan et. al described an enteric-coated NPs incorporated with focal adhesion kinase inhibitor administered orally that showed decrease in tumor volume as compared to other controls in this study111 . Although the active targeting to the BBB by systemic administration is a promising method of drug delivery to GBM, most of the FDA approved or undergoing clinical trials are the ones that are passively targeted[112][113][114][115][116] .…”

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confidence: 87%

Harnessing nanomedicine for therapeutic intervention in glioblastoma

Gutkin

Peer

2016

Expert Opinion on Drug Delivery

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Glioblastoma is a type of brain cancer arises from glial cells. Glioblastoma multiforme (GBM), a subtype of glioblastoma, is the most common and most aggressive primary brain tumor. Currently, GBM therapy includes surgery and post-operative high-doses of radiation and chemotherapy. This therapeutic strategy has a limited contribution in extending the survival rate of GBM patients. Areas covered: Herein, we focus on harnessing nanoscale drug delivery strategies to treat brain malignancies. Specifically, we briefly discuss the challenges facing GBM therapy such as restricted passage across the blood-brain barrier (BBB) and low enhanced permeability and retention effect. Next, we describe different pathways to address these challenges. Finally, we discuss the field of nanomedicine, which emerged as a promising platform for drug delivery to brain malignancies. Expert opinion: Countless strategies have been applied in preclinical and clinical settings to treat GBM. Among them is the use of different types of nanoparticles (NPs) and viruses with different approaches to cross or bypass the BBB. We suggest here a paradigm shift in thinking about crossing the BBB and tumor penetration as fundamental issues that need to be address in order to improve the therapeutic outcome in GBM.

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A focal adhesion kinase inhibitor 16-hydroxy-cleroda-3,13-dien-16,15-olide incorporated into enteric-coated nanoparticles for controlled anti-glioma drug delivery

Cited by 21 publications

References 47 publications

16-hydroxy-cleroda-3,13-dien-16,15-olide induced glioma cell autophagy via ROS generation and activation of p38 MAPK and ERK-1/2

16-hydroxy-cleroda-3,13-dien-16,15-olide induced glioma cell autophagy via ROS generation and activation of p38 MAPK and ERK-1/2

Encapsulation of 16-Hydroxycleroda-3,13-Dine-16,15-Olide in Mesoporous Silica Nanoparticles as a Natural Dipeptidyl Peptidase-4 Inhibitor Potentiated Hypoglycemia in Diabetic Mice

Harnessing nanomedicine for therapeutic intervention in glioblastoma

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