Neuroprotective Effects of Nipradilol on Purified Cultured Retinal Ganglion Cells

2002 ◽  
Vol 11 (3) ◽  
pp. 231-238 ◽  
Author(s):  
Kenji Kashiwagi ◽  
Yoko Iizuka ◽  
Shigeo Tsukahara
2010 ◽  
Vol 51 (7) ◽  
pp. 3544 ◽  
Author(s):  
Jia Ma ◽  
Wenhan Yu ◽  
Yun Wang ◽  
Guiqun Cao ◽  
Suping Cai ◽  
...  

2006 ◽  
Vol 3 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Yuta Inokuchi ◽  
Masamitsu Shimazawa ◽  
Yoshimi Nakajima ◽  
Shinsuke Suemori ◽  
Satoshi Mishima ◽  
...  

Propolis, a honeybee product, has gained popularity as a food and alternative medicine. Its constituents have been shown to exert pharmacological (anticancer, antimicrobial and anti-inflammatory) effects. We investigated whether Brazilian green propolis exerts neuroprotective effects in the retinain vitroand/orin vivo.In vitro, retinal damage was induced by 24 h hydrogen peroxide (H2O2) exposure, and cell viability was measured by Hoechst 33342 and YO-PRO-1 staining or by a resazurin–reduction assay. Propolis inhibited the neurotoxicity and apoptosis induced in cultured retinal ganglion cells (RGC-5, a rat ganglion cell line transformed using E1A virus) by 24 h H2O2 exposure. Propolis also inhibited the neurotoxicity induced in RGC-5 cultures by staurosporine. Regarding the possible underlying mechanism, in pig retina homogenates propolis protected against oxidative stress (lipid peroxidation), as also did trolox (water-soluble vitamin E). In micein vivo, propolis (100 mg kg−1; intraperitoneally administered four times) reduced the retinal damage (decrease in retinal ganglion cells and in thickness of inner plexiform layer) induced by intravitrealin vivo N-methyl-d-aspartate injection. These findings indicate that Brazilian green propolis has neuroprotective effects against retinal damage bothin vitroandin vivo, and that a propolis-induced inhibition of oxidative stress may be partly responsible for these neuroprotective effects.


2009 ◽  
Vol 1251 ◽  
pp. 269-275 ◽  
Author(s):  
Masamitsu Shimazawa ◽  
Yoshimi Nakajima ◽  
Yukihiko Mashima ◽  
Hideaki Hara

2005 ◽  
Vol 1050 (1-2) ◽  
pp. 15-26 ◽  
Author(s):  
Makiko Yamasaki ◽  
Hiromu K. Mishima ◽  
Hidetoshi Yamashita ◽  
Kenji Kashiwagi ◽  
Kazuhiko Murata ◽  
...  

2016 ◽  
Vol 139 (2) ◽  
pp. 256-269 ◽  
Author(s):  
Katharina Bell ◽  
Corina Wilding ◽  
Sebastian Funke ◽  
Natarajan Perumal ◽  
Sabine Beck ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Peter Heiduschka ◽  
Daniel Renninger ◽  
Dietmar Fischer ◽  
Adrienne Müller ◽  
Sabine Hofmeister ◽  
...  

Lens injury induced activation of retinal glia, and subsequent release of ciliary neurotrophic factor (CNTF) and leukaemia inhibitory factor (LIF) potently protect axotomised retinal ganglion cells from apoptosis and promotes axon regeneration in the injured optic nerve. The goal of the current study was to investigate if similar effects may also be applicable to rescue photoreceptors from degeneration in a model of retinitis pigmentosa. Lens injury was performed in the Royal College of Surgeons (RCS) rats at the age of one month. The survival of photoreceptors was evaluated histologically, and retinal function was analysed by electroretinography (ERG). Expression of CNTF was also analysed. Lens injury significantly enhanced the survival of photoreceptors 1 month after surgery compared to untreated controls, which was associated with an enhanced ERG response. In addition, lens injury significantly protected photoreceptors from degeneration in the contralateral eye, although to a much lesser extent. We could show that lens injury is sufficient to transiently delay the degeneration of photoreceptors in the RCS rat. The observed neuroprotective effects may be at least partially mediated by an upregulation of CNTF expression seen after lens injury.


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