Latanoprost Exerts Neuroprotective Activity in vitro and in vivo

Drago, Filippo; Valzelli, Stefano; Emmi, I.; Marino, Antonio; Scalia, Cristina Cassar; Marino, V.

doi:10.1006/exer.2000.0975

Cited by 45 publications

(25 citation statements)

References 27 publications

(35 reference statements)

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“…However, Drago et al clearly documented that latanoprost may protect retinal cells agains glutamate toxicity at particular concentrations, probably through the blockade of glutamate receptors. They speculated that the in vivo neuroprotective activity of PGA may be the result of multiple actions on different biological targets [10]. In our study, probably inhibition of these pathways with PGA yielded significantly lower levels of XO in the vitreous.…”

Section: Discussionsupporting

confidence: 53%

“…Even though this can be accepted as a coincidence, a relatively high affinity of a particular PGA to certain retinal cells and layers is another possibility. Moreover, as mentioned by Drago et al, the in vivo neuroprotective potential of these agents could be the result of multiple actions on different biological targets and their variable potency on different targets could be related to their chemical compositions [10].…”

Section: Discussionmentioning

confidence: 99%

“…There are currently three internationally approved analogues (bimatoprost, latanoprost, and travoprost) for the treatment of patients with elevated intraocular pressure. In addition to the IOP lowering effect, a recent paper documented the retinal cell protective potential against ischemic conditions, in vivo and in vitro for latanoprost [10]. Clinically apoptosis has been shown to occur in retinas with glaucoma [27].…”

Section: Introductionmentioning

confidence: 99%

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Comparison of the Protective Effects of Prostaglandin Analogues in the Ischemia and Reperfusion Model of Rabbit Eyes

et al. 2009

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This study was planned to investigate the neuroprotective potentials of three commercially available prostaglandin analogues (PGA), in the ischemia and reperfusion model (I/R). Thirty New Zealand rabbits were divided into 5 groups and except for the control group (non-ischemic, non-treated), 0.9% NaCl, bimatoprost, latanoprost, or travoprost were applied to both eyes of animals of the respective groups for 1 week. At the end of treatment, ischemia was induced in both eyes of the 4 treatment groups by anterior chamber irrigation of the animals for 60 min. Following 24 h reperfusion, the animals were sacrified. Enucleated eyes and retinal tissues were investigated by light microscopy, electron microscopy, immunohistochemicstry for retinal histopathology, intracellular and apoptotic cells and by retinal morphometry. Vitreous samples were biochemically investigated for probable role of reactive oxygen species, by measuring xanthine oxidase (XO) activity. Analysis of morphometric measurements and vitreous XO activity revealed significant differences between the PGAtreated groups and the NaCl-treated group (P<0.05). Similarly, apoptotic cell counts in different retinal layers showed that PGA-treated groups had fewer apoptotic cells in all retinal layers than the NaCl-treated ischemic group (P<0.05). PGA may have high protective potential for different retinal layers and cells. Biochemical analysis of vitreous showed that all PGAs decreased vitreous XO activity significantly compared to the NaCl-treated group (P<0.05). However we could not find any statistically significant differences among the analogues. PGAs may reduce the injury induced by I/R, through the inhibition of XO activity, and it seems that their effects are elicited through numerous pathways.

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Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Comparison of the Protective Effects of Prostaglandin Analogues in the Ischemia and Reperfusion Model of Rabbit Eyes

et al. 2009

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“…As for the neuroprotective activities of latanoprost on retinal cells, Drago et al reported that lactate accumulation in the retina induced by ischemia-reperfusion injury would be suppressed by intraperitoneal administration of latanoprost [10]. It was also reported that the susceptive damaged neurons by ischemia-reperfusion injury were not only RGCs but also amacrine cells [31].…”

Section: Discussionmentioning

confidence: 99%

“…Taking these findings together, we postulated that latanoprost stimulates the FP receptor in RGCs and leads to a neuroprotective effect against glaucoma-induced RGC damage. Only one study has reported the neuroprotective effect of intraperitoneal injection of latanoprost on the retina damaged by ischemia-reperfusion in vivo [10]. However, the effect of intraocular administration of latanoprost on injured RGC, including NMDA injury or optic nerve axotomy, which has similar gene expressional changes to glaucoma [2,3], has not been investigated.…”

Section: Introductionmentioning

confidence: 99%