June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Neuroprotective effect on the retinal ganglion cells by brimonidine loaded HSA nanoparticles in the acute optic nerve crush model
Author Affiliations & Notes
  • Hyuncheol Kim
    Department of Chemical and Biomolecular Engineering, Sogang University, Seoul, Republic of Korea
  • Hyungwon Moon
    Department of Chemical and Biomolecular Engineering, Sogang University, Seoul, Republic of Korea
  • Kyoung Nam Kim
    Department of Ophthalmology, Seoul National University College of Medicine, Seoul, Republic of Korea
  • Yu Jeong Kim
    Department of Ophthalmology, Seoul National University College of Medicine, Seoul, Republic of Korea
  • Jin Wook Jeoung
    Department of Ophthalmology, Seoul National University College of Medicine, Seoul, Republic of Korea
  • Ki Ho Park
    Department of Ophthalmology, Seoul National University College of Medicine, Seoul, Republic of Korea
  • Footnotes
    Commercial Relationships Hyuncheol Kim, None; Hyungwon Moon, None; Kyoung Nam Kim, None; Yu Jeong Kim, None; Jin Wook Jeoung, None; Ki Ho Park, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 1094. doi:
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      Hyuncheol Kim, Hyungwon Moon, Kyoung Nam Kim, Yu Jeong Kim, Jin Wook Jeoung, Ki Ho Park; Neuroprotective effect on the retinal ganglion cells by brimonidine loaded HSA nanoparticles in the acute optic nerve crush model. Invest. Ophthalmol. Vis. Sci. 2013;54(15):1094.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: To examine the neuroprotective effect of α2-agonist brimonidine loaded human serum albumin (HSA) nanoparticles on the survival of retinal ganglion cells after acute optic nerve crush.

Methods: Brimonidine loaded HSA nanoparticles were fabricated by desolvation technique. The size distribution and zeta potential were evaluated by dynamic light scattering method. The loaded amount and in vitro release rate of brimonidine from the HSA nanoparticles were determined with the HPLC. Acute optic nerve crush was induced by clipping the optic nerve for 60s. After optic nerve injury, brimonidine loaded HSA nanoparticles, free HSA nanoparticles, and balance salt solution (BSS) control were adiministered intravitreally. Retinal ganglion cell loss was evalulated by cell count in a retinal flat mount, which was visualized by the retrograde transport of rhodamin-dextran 3000. Retinal ganglion cell loss was determined 5 days post administration.

Results: The brimonidine loaded HSA nanoparticles showed narrow size distribution and negatively charged surface to be 152.78 +/- 51.1 nm and -29.7 +/- 7.52 mV, respectively. The concentration of brimonidine in HSA nanoparticles was 214.12 μg/mL and consistently released for over 5 days. In the neuroprotection analysis, compared to the uncrush retinal ganglion cells (control group), the BSS treated group described the retinal ganglion cell loss of 66.81 +/- 4.34 % (P<0.05). However, retinal ganglion cell loss in the brimonidine - HSA nanoparticle treated group showed 26.19 +/- 5.21% (P<0.05 vs. control group) at the dose of 8.78 μg (brimonidine). Retinal ganglion cell loss was decreased more than 2 times, compared to the BSS treated group 5 days post administration.

Conclusions: Brimonidine loaded HSA nanoparticles delivered neuroprotective glaucomatous drugs to the retina and described the neuroprotective effect on the retinal ganglion cells effectively.

Keywords: 608 nanomedicine • 615 neuroprotection  
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