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Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Biomater+Sci 2019 ; 7 (4): 1554-1564 Nephropedia Template TP
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A stimuli-responsive drug release nanoplatform for kidney-specific anti-fibrosis treatment #MMPMID30681674
Tan L; Lai X; Zhang M; Zeng T; Liu Y; Deng X; Qiu M; Li J; Zhou G; Yu M; Geng X; Hu J; Li A
Biomater Sci 2019[Mar]; 7 (4): 1554-1564 PMID30681674show ga
The renoprotective effects of hypoxia inducible-factor (HIF) activators have been demonstrated by improving renal hypoxia in chronic kidney disease. Cobalt chloride is one of the most widely used HIF activators in biomedicine; however, poor kidney targeting and undesirable side effects greatly limit its clinical applications. Here, we report a novel stimuli-responsive drug release nanoplatform in which glutathione (GSH)-modified Au nanoparticles (GLAuNPs) and Co2+ self-assemble into nanoassemblies (GLAuNPs-Co) through coordination interactions between empty orbitals of Co2+ and lone pairs of GSH. The GLAuNPs, when used as a drug carrier, demonstrated high drug loading capacity and pH-triggered drug release after assembling with Co2+. The acidic environment of lysosomes in renal fibrosis tissues could disassemble GLAuNPs-Co and release Co2+. Moreover, encapsulation of the Co2+ ions in the GLAuNPs greatly lowered the cytotoxicity of Co2+ in kidney tubule cells. Tissue fluorescence imaging showed that GLAuNPs-Co specifically accumulated in the kidneys, especially in the renal proximal tubules. After GLAuNPs-Co was intraperitoneally injected into ureter-obstructed mice, significant attenuation of interstitial fibrosis was exhibited. The beneficial effects can be mainly ascribed to miR-29c expression restored by HIF-alpha activation. These findings revealed that GLAuNPs-Co have pH-responsive drug release and renal targeting capabilities; thus, they are a promising drug delivery platform for treating kidney disease.
Biomater+Sci 2019 ; 7 (4): 1554-1564
