Effects of prenatal exposure to diclofenac sodium and saline on the optic nerve of 4- and 20-week-old male rats: a stereological and histological study

Çolakoğlu, Serdar; Aktaş, Abit; Raimondo, Stefania; Türkmen, Aysın Pinar; Bz, Altunkaynak; Odacı, Ersan; Geuna, Stefano; Kaplan, Süleyman

doi:10.3109/10520295.2013.827741

Cited by 7 publications

(3 citation statements)

References 54 publications

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“…However, axonal assessment only in the distal part means ignoring the axon outgrowths, which originate from the proximal part. Thus, axon outgrowths, which develop as a response to exogenous neurotrophic factor treatment, are insufficient to estimate direct information about the accurate number of axotomized neurons (51,53,54). Briefly, combined quantitative evaluations will give more precise information about regeneration.…”

Section: Regenerative Events Following Damagementioning

confidence: 99%

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The role of growth factors in nerve regeneration

Önger

Delibaş

Türkmen

et al. 2016

DD&T

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Section: Regenerative Events Following Damagementioning

confidence: 99%

“…In the evaluation of peripheral nerve regeneration, total number of axons in the distal part of nerve and functional tests are used (50)(51)(52). However, axonal assessment only in the distal part means ignoring the axon outgrowths, which originate from the proximal part.…”

Section: Regenerative Events Following Damagementioning

confidence: 99%

The role of growth factors in nerve regeneration

Önger

Delibaş

Türkmen

et al. 2016

DD&T

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“…Diclofenac is another widely used NSAID as an analgesic and anti-inflammatory. In nerve regeneration, diclofenac has been found to have conflicting effects by both improving regeneration but also having harmful effects on developing nerves [38][39][40][41]. Diclofenac has been shown to be teratogenic; during the embryonic period, the number of nerve fibers and the cross-sectional area of axons in developing sciatic nerves were affected when exposed to diclofenac [39].…”

Section: Discussionmentioning

confidence: 99%

Exploring the Nerve Regenerative Capacity of Compounds with Differing Affinity for PPARγ In Vitro and In Vivo

Rayner

Kellaway

Kingston

et al. 2022

Cells

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Damage to peripheral nerves can cause debilitating consequences for patients such as lifelong pain and disability. At present, no drug treatments are routinely given in the clinic following a peripheral nerve injury (PNI) to improve regeneration and remyelination of damaged nerves. Appropriately targeted therapeutic agents have the potential to be used at different stages following nerve damage, e.g., to maintain Schwann cell viability, induce and sustain a repair phenotype to support axonal growth, or promote remyelination. The development of therapies to promote nerve regeneration is currently of high interest to researchers, however, translation to the clinic of drug therapies for PNI is still lacking. Studying the effect of PPARγ agonists for treatment of peripheral nerve injures has demonstrated significant benefits. Ibuprofen, a non-steroidal anti-inflammatory drug (NSAID), has reproducibly demonstrated benefits in vitro and in vivo, suggested to be due to its agonist action on PPARγ. Other NSAIDs have demonstrated differing levels of PPARγ activation based upon their affinity. Therefore, it was of interest to determine whether affinity for PPARγ of selected drugs corresponded to an increase in regeneration. A 3D co-culture in vitro model identified some correlation between these two properties. However, when the drug treatments were screened in vivo, in a crush injury model in a rat sciatic nerve, the same correlation was not apparent. Further differences were observed between capacity to increase axon number and improvement in functional recovery. Despite there not being a clear correlation between affinity and size of effect on regeneration, all selected PPARγ agonists improved regeneration, providing a panel of compounds that could be explored for use in the treatment of PNI.

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As a painkiller: a review of pre- and postnatal non-steroidal anti-inflammatory drug exposure effects on the nervous systems

Yurt

Kaplan

2017

Inflammopharmacol

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Diclofenac sodium (DS) is commonly used for the treatment of acute and chronic pain, even for extended periods of time. Over the years, DS has been associated with toxicity in nervous tissue, in addition to its anti-inflammatory properties. Basic neurobiological research has enhanced our understanding of the biological and pathological outcomes of toxicity. Several studies have suggested DS-induced cytotoxicity in the nervous system. Prenatal toxicities of DS are thought to be capable of leading to postnatal defects. This review describes the morphoquantitative, histological and pathological effects of DS on the central and peripheral nervous systems. Knowledge of these effects may assist with the development of a suitable therapeutic approach. In addition, understanding the mechanism of DS-dependent neuronal impairments may contribute to selection of appropriate antioxidant therapy.

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Effects of prenatal exposure to diclofenac sodium and saline on the optic nerve of 4- and 20-week-old male rats: a stereological and histological study

Cited by 7 publications

References 54 publications

The role of growth factors in nerve regeneration

The role of growth factors in nerve regeneration

Exploring the Nerve Regenerative Capacity of Compounds with Differing Affinity for PPARγ In Vitro and In Vivo

As a painkiller: a review of pre- and postnatal non-steroidal anti-inflammatory drug exposure effects on the nervous systems

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