Size and temporal-dependent efficacy of oltipraz-loaded PLGA nanoparticles for treatment of acute kidney injury and fibrosis

H, Yu; Lin, Tong; Chen, Wei; Cao, Wenmin; Zhang, Chengwei; Wang, Tianwei; Ding, Meng; Zhao, Sheng; Wei, Hui; Guo, Hongqian; Zhao, Xiaozhi

doi:10.1016/j.biomaterials.2019.119368

Cited by 83 publications

(81 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For the control conditions, 45 μ M mannitol was used to match the hyperosmolality of the cells cultured in the hyperglycemic conditions. The glucose concentrations and oltipraz concentrations used in the present study were based on previous studies [ 15 , 31 ].…”

Section: Methodsmentioning

confidence: 99%

“…Oltipraz activates Nrf2 and subsequently increases the expression of genes encoding antioxidants. Oltipraz has been shown to be effective in animal models of certain diseases due to its antioxidant properties, including heart failure, acute kidney injury, and liver injury [30][31][32]. Therefore, oltipraz may potentially inhibit SC apoptosis by preventing oxidative stress.…”

Section: Biomed Research Internationalmentioning

confidence: 99%

“…Nrf2 functions as an activator of antioxidant response element (ARE), which is recognized as the cis-element essential for the basal and inducible expression of several antioxidant genes, including NADPH quinone oxidoreductase 1 (NQO-1) [25][26][27]. Oltipraz and its oxidized metabolites have proven strong antioxidant effects in animal models or clinical patients in certain diseases [28][29][30][31][32]. However, it is still unclear whether oltipraz may reduce apoptosis of SCs through reducing oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Oltipraz Prevents High Glucose-Induced Oxidative Stress and Apoptosis in RSC96 Cells through the Nrf2/NQO1 Signalling Pathway

Jiang

Bian

et al. 2020

BioMed Research International

View full text Add to dashboard Cite

Diabetic peripheral neuropathy (DPN) is a common complication of diabetes mellitus (DM). Schwann cell (SC) apoptosis contributes to the occurrence and development of DPN. Effective drugs to prevent SC apoptosis are required to relieve and reverse peripheral nerve injury caused by DM. Oltipraz [4-methyl-5-(2-pyrazinyl)-1,2-dithiole-3-thione], an agonist of nuclear factor erythroid derived-2-related factor 2 (Nrf2), exerts strong effect against oxidative stress in animal models or clinical patients in certain diseases, including heart failure, acute kidney injury, and liver injury. The aim of the present study was to determine the effectiveness of oltipraz in preventing SC apoptosis induced by high glucose levels. RSC96 cells pretreated with oltipraz were cultured in high-glucose medium (50 mM glucose) for 24 h, and cells cultured in medium containing 5 mM glucose were used as the control. Flow cytometry was used to evaluate the degree of apoptosis. A Cell Counting Kit-8 assay was used to assess cell viability. The mitochondrial membrane potential was assessed using JC-1 staining, and reactive oxygen species (ROS) generation was measured using 20,70-dichlorodihydrofluorescein diacetate staining. In addition, the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) levels were also evaluated using the corresponding kits. Flow cytometry was subsequently used to detect apoptosis, and western blotting was used to measure the expression levels of nuclear factor erythroid derived-2-related factor 2 and NADPH quinone oxidoreductase 1. The results showed that high glucose concentration increased oxidative stress and apoptosis in RSC96 cells. Oltipraz improved cell viability and reduced apoptosis of RSC96 cells in the high glucose environment. Additionally, oltipraz exhibited a significant antioxidative effect, as shown by the decrease in MDA levels, increased SOD levels, and reduced ROS generation in RSC96 cells. The results of the present study suggest that oltipraz exhibits potential as an effective drug for treatment with DPN.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Biomed Research Internationalmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Oltipraz Prevents High Glucose-Induced Oxidative Stress and Apoptosis in RSC96 Cells through the Nrf2/NQO1 Signalling Pathway

Jiang

Bian

et al. 2020

BioMed Research International

View full text Add to dashboard Cite

show abstract

“…AKI is mainly caused by sepsis, ischemia-reperfusion, and/or nephrotoxicity, and it is characterized by rapid progression of inflammation and oxidative stress. Different drug delivery systems have recently been explored for AKI therapy in murine models, including drug conjugates [ 304 ], micelles [ 305 ], nanoparticles [ 306 ], microspheres [ 307 ], and injectable hydrogels [ 308 ]. Of note, Ji and Du et al designed pH-responsive and AKI-kidney targeting nanopolyplexes by electrostatic forces between anionic hyaluronic acid and cationic chitosan for effective delivery of SS-31 (a mitochondrial targeting peptide with potent antioxidant activity) to treat AKI.…”

Section: Treatment Of Inflammatory Diseases By Bioresponsive Drug Delmentioning

confidence: 99%

Bioresponsive drug delivery systems for the treatment of inflammatory diseases

Ding

et al. 2020

Journal of Controlled Release

121

View full text Add to dashboard Cite

Inflammation is intimately related to the pathogenesis of numerous acute and chronic diseases like cardiovascular disease, inflammatory bowel disease, rheumatoid arthritis, and neurodegenerative diseases. Therefore anti-inflammatory therapy is a very promising strategy for the prevention and treatment of these inflammatory diseases. To overcome the shortcomings of existing anti-inflammatory agents and their traditional formulations, such as nonspecific tissue distribution and uncontrolled drug release, bioresponsive drug delivery systems have received much attention in recent years. In this review, we first provide a brief introduction of the pathogenesis of inflammation, with an emphasis on representative inflammatory cells and mediators in inflammatory microenvironments that serve as pathological fundamentals for rational design of bioresponsive carriers. Then we discuss different materials and delivery systems responsive to inflammation-associated biochemical signals, such as pH, reactive oxygen species, and specific enzymes. Also, applications of various bioresponsive drug delivery systems in the treatment of typical acute and chronic inflammatory diseases are described. Finally, crucial challenges in the future development and clinical translation of bioresponsive anti-inflammatory drug delivery systems are highlighted.

show abstract

“…Interestingly, various methods are in practice for the fabrication of PLGA-NPs, but the most successful one is determined by many drug-related factors (partition, solubility, and coefficient) and based on the nature of polymers (molecular weight, composition, and chemical functional groups) 18, 19 . Hence, single and double emulsion, solvent evaporation, porous glass membrane emulsification, and spray-drying are commonly applied techniques for synthesis of biodegradable PLGA-NPs 20–22 . However, each of these methods have some limitations including particle-size polydispersity, low drug-loading, and encapsulation efficiency and hydrophilic drugs incorporation, etc.…”

Section: Introductionmentioning

confidence: 99%

Brinzolamide loaded core-shell nanoparticles for enhanced coronial penetration in the treatment of glaucoma

Song

Zhang

2020

Journal of Applied Biomaterials & Functional Materials

View full text Add to dashboard Cite

A neurodegenerative disorder, glaucoma is a leading cause of blindness in the world. The conventional treatment strategies do not allow the significant penetration of the drug in the cornea. Therefore, we prepare a brinzolamide (Brz) loaded core-shell nanoparticles (NPs) to enhance the coronial penetration of the drug and thus treating the glaucoma. The shell of the NPs was composed of phosphatidylserine (PS; 1,2-diacyl-sn-glycero-3-phospho-L-serine), whereas the core of the NPs contains the Brz encapsulated in brinzolamide–phosphatidylserine–polymer poly-(DL-lactic acid-co-glycolic acid)–phosphatidylserine (Brz-PS-PLGA). The synthesis of Brz-PS-PLGA was achieved by using a coaxial electrospray process (CEP), which allows the preparation of the particles in a single step. The size of Brz-PS-PLGA with PS shell and brinzolamide–poly (lactic-co-glycolic) acid (Brz-PLGA) without shell was 571 ± 27.02 nm and 456 ± 19.17 nm, respectively. The charges on the surface of Brz-PS-PLGA and Brz-PLGA were (-) 27.45 ± 2.98 mV and (-) 19.47 ± 2.83 mV. The transmission electron microscopy images clearly reveal the PS shell as a light black layer over the dark black PLGA core. The CEP allows the high encapsulation of Brz in Brz-PS-PLGA where percentage of entrapment efficiency for Brz-PS-PLGA was 88.13 ± 6.43%. The release study conducted in a simulated tear fluid revealed the sustained release patterns of Brz from Brz-PS-PLGA and these were nontoxic to the cells as revealed by the cytotoxicity studies. Further, the Brz-PS-PLGA enhanced the coronial penetration of Brz and was capable of significantly reducing the intraocular pressure (IOP) after administration to the rabbit eye in comparison to the Brz-PLGA and free Brz. The results clearly suggest that the PS coating significantly enhances the capability of the particles in reducing IOP.

show abstract

Size and temporal-dependent efficacy of oltipraz-loaded PLGA nanoparticles for treatment of acute kidney injury and fibrosis

Cited by 83 publications

References 40 publications

Oltipraz Prevents High Glucose-Induced Oxidative Stress and Apoptosis in RSC96 Cells through the Nrf2/NQO1 Signalling Pathway

Oltipraz Prevents High Glucose-Induced Oxidative Stress and Apoptosis in RSC96 Cells through the Nrf2/NQO1 Signalling Pathway

Bioresponsive drug delivery systems for the treatment of inflammatory diseases

Brinzolamide loaded core-shell nanoparticles for enhanced coronial penetration in the treatment of glaucoma

Contact Info

Product

Resources

About