Protection of Rat Retina from Ischemia-Reperfusion Injury by Vasoactive Intestinal Peptide (VIP): The Effect of VIP on Lipid Peroxidation and Antioxidant Enzyme Activity of Retina and Choroid

Tunçel, Neşe; Başmak, Hikmet; Uzuner, Kubi̇lay; Tunçel, Muzaffer; Altıokka, Göksel; Zaimoğlu, V.; Özer, Ahmet; Gürer, Fi̇rdevs

doi:10.1111/j.1749-6632.1996.tb17509.x

Cited by 30 publications

(18 citation statements)

References 14 publications

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“…Our present results confirm that PACAP is able to protect not only inner retinal layers but also photoreceptors. In addition to PAC1 receptors, the involvement of VPAC receptors cannot be excluded in the observed protective effects since VIP has also been described to be retinoprotective in an ischemia-reperfusion injury (Tuncel et al 1996). In addition to the neuroprotection, in the present study we also observed that PACAP decreased the significant edema formation in the retina 7 days after irradiation.…”

Section: Discussionsupporting

confidence: 47%

Effects of PACAP in UV-A Radiation-Induced Retinal Degeneration Models in Rats

et al. 2010

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The retina is constantly exposed to ultraviolet (UV) light with different wavelengths, which may lead to chronic UV-induced retinal injury. In our previous studies, we have shown the protective effects of pituitary adenylate cyclase activating polypeptide (PACAP) in toxic and ischemic retinal injuries. The aim of the present study was to investigate the effects of PACAP in UV-A-induced retinal lesion. We used diffuse UV-A radiation (315-400 nm) to induce acute retinal damage over a short period of exposure. Using standard histological (morphological and morphometrical) analysis, we assessed the actions of intravitreal PACAP (100 pmol/5 µl) treatment on acute UV-A-induced retinal damage. We measured the thickness of nuclear and plexiform layers as well as the number of cells in the outer nuclear and inner nuclear layers and in the ganglion cell layer. Outer limiting membrane-inner limiting membrane distances in the cross-section of the retina were also examined. Our results show that UV-A light-induced retinal damage led to severe degeneration in the photoreceptor layer, and in the outer and inner nuclear layers. Alteration in the plexiform layers was also observed. We found that post-irradiation PACAP treatment significantly attenuated the UV-A-induced retinal damage. Our results provide the basis for future clinical application of PACAP treatment in retinal degeneration and may have clinical implications in several ophthalmic diseases.

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Section: Discussionsupporting

confidence: 47%

Effects of PACAP in UV-A Radiation-Induced Retinal Degeneration Models in Rats

et al. 2010

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“…In addition, effects via the common VIP/PACAP receptors (VPAC1 and VPAC2) cannot be excluded, since these receptors are also present in the retina . Although the cAMP increasing effects of VIP is much less pronounced in various tissues, including the retina (Olianas et al, 1997;Shoge et al, 1999), protective effects of VIP in retinal ischemia/reperfusion injury and in vitro glutamate-toxicity have been demonstrated (Tuncel et al, 1996;Shoge et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Degree of damage compensation by various pacap treatments in monosodium glutamate-induced retinal degeneration

et al. 2005

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Pituitary adenylate cyclase activating polypeptide (PACAP) has been shown to be neuroprotective in retinal ischemia and monosodium L-glutamate (MSG)-induced retinal degeneration. Here we describe how different MSG treatments (1x and 3x application) cause retinal damage and finally lead to the destruction of the entire inner retina and how PACAP attenuates this effect. Newborn rats from both sexes were injected subcutaneously with 2 mg/g bodyweight MSG on postnatal days 1, 5 and 9. The left eye was left intact while we injected 5 microl PACAP38 solution (100 pmol) into the vitreous of the right eye with a Hamilton syringe at the time of (i) the first, (ii) the first two or (iii) all three MSG injections. Histological analysis has shown that the above described MSG treatment caused the entire inner plexiform layer (IPL) to degenerate, and the inner nuclear (INL) and ganglion cell layers (GCL) seemed fused. One time PACAP38 treatment at the first MSG application did not change the degenerative capacity of MSG. However, if animals received PACAP38 into the vitreous of the eye at the first 2 or all 3 times, a substantial protective effect could be observed. The IPL remained well discernible, the INL retained 2-3 cell rows and the number of cells in the GCL was substantially higher than in the MSG-treated retinas, and was not significantly different from that observed in the control tissue. We conclude that (i) 2 or 3 times PACAP treatment attenuates retinal degeneration; (ii) one PACAP treatment does not provide protection against repeated excitotoxic insults, and (iii) repeated application of PACAP under these experimental conditions may lead to a primed state in which further neurotoxic insults are ineffective.

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“…At the biochemical level, increased DNA fragmentation is a distinctive feature of apoptosis, and MDA is a measure of lipid peroxidation (Collins et al 1997). Although the antioxidant, anti-apoptotic, and anti-inflammatory effectiveness of VIP has been well documented in various tissue and pathological conditions, this is the first report demonstrating the antioxidant and anti-apoptotic activity of VIP in the corpus striatum of 6-OHDA-lesioned rats (Kalfin et al 1993;Said et al 1995Said et al , 1996Tunçel et al 1996Tunçel et al , 1997Tunçel et al , 1998Uzuner et al 1995;Gomariz et al 2001).…”

Section: Discussionmentioning

confidence: 98%

“…Inhibition of proapoptotic caspase and poly-ADP ribose polymerase (PARP), as well as the upregulation of bcl-2 protein expression, increased cell viability in many tissues (Said 2000). VIP, either by scavenging or by inhibiting the production of ROS, can protect these tissues against oxidative stress (Kalfin et al 1993;Tunçel et al 1996Tunçel et al , 1997Tunçel et al , 1998Uzuner et al 1995).…”

Section: Discussionmentioning

confidence: 99%

“…These effects, along with VIP's anti-glutamatergic function, have been well documented in various tissues, including neural tissue, and in pathological conditions such as PD, septic shock, hemorrhagic shock, rheumatoid arthritis, acute respiratory distress syndrome, ischemic-reperfused retina, and brain trauma (Tunçel et al 1996(Tunçel et al , 1997(Tunçel et al , 1998(Tunçel et al , 2005Delgado and Ganea 2003a;Can et al 2004;Gonzalez-Rey et al 2005;Korkmaz et al 2010). VIP can also cross the blood-brain barrier (BBB; Dogrukol-Ak et al 2003).…”

Section: Introductionmentioning

confidence: 99%

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Antioxidant and Anti-Apoptotic Activity of Vasoactive Intestinal Peptide (VIP) Against 6-Hydroxy Dopamine Toxicity in the Rat Corpus Striatum

et al. 2011

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6-Hydroxydopamine (6-OHDA) is an oxidative stress neurotoxin, which is oxidized in neurons, causes respiratory inhibition, and induces free radical formation and oxidative stress. Therefore, a 6-OHDA-induced Parkinson's disease (PD) experimental model can be used to test a candidate molecule for use as an antioxidant that could be a promising therapeutic for treating Parkinson's disease. Recent studies have shown that vasoactive intestinal peptide (VIP) might be a good candidate agent for the treatment of PD. In this study, the anti-apoptotic and antioxidant actions of VIP were investigated using the 6-OHDA-lesioned rat model for PD. Twenty-four young adult Sprague-Dawley rats were used. The rats were separated into the following groups: group I (n = 8), sham operated; group II (n = 8), 6-OHDA lesioned; group III (n = 8), 6-OHDA lesioned + i.p. VIP-injected (25 ng/kg) every 2 days for 15 days. The first i.p. injection of VIP was made 1 h after the intrastriatal 6-OHDA microinjection. Antioxidant enzymatic activity [super oxide dismutase (SOD) and catalase (CAT)], lipid peroxidation, nitric oxide and DNA fragmentation were measured from homogenates isolated from the corpus striatum. SOD, CAT, malondialdehyde, and DNA fragmentation were measured using a spectrophotometer, and nitric oxide (NO) levels were measured by capillary electrophoresis. 6-OHDA significantly induced oxidative stress, lipid peroxidation, and DNA fragmentation in the corpus striatum of rats. VIP significantly protected neuronal tissue from oxidative stress and apoptosis by reducing lipid peroxidation and DNA fragmentation. 6-OHDA toxicity did not cause significant changes in NO production in the corpus striatum. However, VIP treatment significantly reduced NO levels in brain tissue.

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Protection of Rat Retina from Ischemia-Reperfusion Injury by Vasoactive Intestinal Peptide (VIP): The Effect of VIP on Lipid Peroxidation and Antioxidant Enzyme Activity of Retina and Choroid

Cited by 30 publications

References 14 publications

Effects of PACAP in UV-A Radiation-Induced Retinal Degeneration Models in Rats

Effects of PACAP in UV-A Radiation-Induced Retinal Degeneration Models in Rats

Degree of damage compensation by various pacap treatments in monosodium glutamate-induced retinal degeneration

Antioxidant and Anti-Apoptotic Activity of Vasoactive Intestinal Peptide (VIP) Against 6-Hydroxy Dopamine Toxicity in the Rat Corpus Striatum

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