Melatonin preserves superoxide dismutase activity in hypoglossal motoneurons of adult rats following peripheral nerve injury

Hung Ming Chang, Yi Lun Huang, Chyn Tair Lan, Un In Wu, Ming E. Hu, Su Chung Youn

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Peripheral nerve injury (PNI) produces functional changes in lesioned neurons in which oxidative stress is considered to be the main cause of neuronal damage. As superoxide dismutase (SOD) is an important antioxidative enzyme involved in redox regulation of oxidative stress, the present study determined whether melatonin would exert its beneficial effects by preserving the SOD reactivity following PNI. Adult rats subjected to hypoglossal nerve transection were intraperitoneally injected with melatonin at ones for 3, 7, 14, 30 and 60 days successively. The potential neuroprotective effects of melatonin were quantitatively demonstrated by neuronal nitric oxide synthase (nNOS), mitochondrial manganese SOD (Mn-SOD), and cytosolic copper-zinc SOD (Cu/Zn-SOD) immunohistochemistry. The functional recovery of the lesioned neurons was evaluated by choline acetyltransferase (ChAT) immunohistochemistry along with the electromyographic (EMG) recordings of denervation-induced fibrillation activity. The results indicate that following PNI, the nNOS immunoreactivity was significantly increased in lesioned neurons peaking at 14 days. The up-regulation of nNOS temporally coincided with the reduction of ChAT and SOD in which the Cu/Zn-SOD showed a greater diminution than Mn-SOD. However, following melatonin administration, the nNOS augmentation was successfully suppressed and the activities of Mn-SOD, Cu/Zn-SOD, and ChAT were effectively preserved at all postaxotomy periods. EMG data also showed a decreased fibrillation in melatonin-treated groups, suggesting a potential effect of melatonin in promoting functional recovery. In association with its significant capacity in preserving SOD reactivity, melatonin is suggested to serve as a powerful therapeutic agent for treating PNI-relevant oxidative damage.

Original languageEnglish
Pages (from-to)172-180
Number of pages9
JournalJournal of Pineal Research
Volume44
Issue number2
DOIs
Publication statusPublished - Mar 2008
Externally publishedYes

Fingerprint

Peripheral Nerve Injuries
Motor Neurons
Melatonin
Superoxide Dismutase
Nitric Oxide Synthase Type I
Choline O-Acetyltransferase
Manganese
Neurons
Hypoglossal Nerve Injuries
Oxidative Stress
Immunohistochemistry
Neuroprotective Agents
Denervation
Oxidation-Reduction
Zinc
Copper
Up-Regulation
Enzymes

Keywords

  • Functional recovery
  • Hypoglossal nucleus
  • Melatonin
  • Nitric oxide
  • Peripheral nerve injury
  • Quantitative image analysis
  • Superoxide dismutase

ASJC Scopus subject areas

  • Endocrinology

Cite this

Melatonin preserves superoxide dismutase activity in hypoglossal motoneurons of adult rats following peripheral nerve injury. / Chang, Hung Ming; Huang, Yi Lun; Lan, Chyn Tair; Wu, Un In; Hu, Ming E.; Youn, Su Chung.

In: Journal of Pineal Research, Vol. 44, No. 2, 03.2008, p. 172-180.

Research output: Contribution to journalArticle

Chang, Hung Ming ; Huang, Yi Lun ; Lan, Chyn Tair ; Wu, Un In ; Hu, Ming E. ; Youn, Su Chung. / Melatonin preserves superoxide dismutase activity in hypoglossal motoneurons of adult rats following peripheral nerve injury. In: Journal of Pineal Research. 2008 ; Vol. 44, No. 2. pp. 172-180.
@article{d532a0aa6a6a4b2a882660736c89c683,
title = "Melatonin preserves superoxide dismutase activity in hypoglossal motoneurons of adult rats following peripheral nerve injury",
abstract = "Peripheral nerve injury (PNI) produces functional changes in lesioned neurons in which oxidative stress is considered to be the main cause of neuronal damage. As superoxide dismutase (SOD) is an important antioxidative enzyme involved in redox regulation of oxidative stress, the present study determined whether melatonin would exert its beneficial effects by preserving the SOD reactivity following PNI. Adult rats subjected to hypoglossal nerve transection were intraperitoneally injected with melatonin at ones for 3, 7, 14, 30 and 60 days successively. The potential neuroprotective effects of melatonin were quantitatively demonstrated by neuronal nitric oxide synthase (nNOS), mitochondrial manganese SOD (Mn-SOD), and cytosolic copper-zinc SOD (Cu/Zn-SOD) immunohistochemistry. The functional recovery of the lesioned neurons was evaluated by choline acetyltransferase (ChAT) immunohistochemistry along with the electromyographic (EMG) recordings of denervation-induced fibrillation activity. The results indicate that following PNI, the nNOS immunoreactivity was significantly increased in lesioned neurons peaking at 14 days. The up-regulation of nNOS temporally coincided with the reduction of ChAT and SOD in which the Cu/Zn-SOD showed a greater diminution than Mn-SOD. However, following melatonin administration, the nNOS augmentation was successfully suppressed and the activities of Mn-SOD, Cu/Zn-SOD, and ChAT were effectively preserved at all postaxotomy periods. EMG data also showed a decreased fibrillation in melatonin-treated groups, suggesting a potential effect of melatonin in promoting functional recovery. In association with its significant capacity in preserving SOD reactivity, melatonin is suggested to serve as a powerful therapeutic agent for treating PNI-relevant oxidative damage.",
keywords = "Functional recovery, Hypoglossal nucleus, Melatonin, Nitric oxide, Peripheral nerve injury, Quantitative image analysis, Superoxide dismutase",
author = "Chang, {Hung Ming} and Huang, {Yi Lun} and Lan, {Chyn Tair} and Wu, {Un In} and Hu, {Ming E.} and Youn, {Su Chung}",
year = "2008",
month = "3",
doi = "10.1111/j.1600-079X.2007.00505.x",
language = "English",
volume = "44",
pages = "172--180",
journal = "Journal of Pineal Research",
issn = "0742-3098",
publisher = "Wiley-Blackwell",
number = "2",

}

TY - JOUR

T1 - Melatonin preserves superoxide dismutase activity in hypoglossal motoneurons of adult rats following peripheral nerve injury

AU - Chang, Hung Ming

AU - Huang, Yi Lun

AU - Lan, Chyn Tair

AU - Wu, Un In

AU - Hu, Ming E.

AU - Youn, Su Chung

PY - 2008/3

Y1 - 2008/3

N2 - Peripheral nerve injury (PNI) produces functional changes in lesioned neurons in which oxidative stress is considered to be the main cause of neuronal damage. As superoxide dismutase (SOD) is an important antioxidative enzyme involved in redox regulation of oxidative stress, the present study determined whether melatonin would exert its beneficial effects by preserving the SOD reactivity following PNI. Adult rats subjected to hypoglossal nerve transection were intraperitoneally injected with melatonin at ones for 3, 7, 14, 30 and 60 days successively. The potential neuroprotective effects of melatonin were quantitatively demonstrated by neuronal nitric oxide synthase (nNOS), mitochondrial manganese SOD (Mn-SOD), and cytosolic copper-zinc SOD (Cu/Zn-SOD) immunohistochemistry. The functional recovery of the lesioned neurons was evaluated by choline acetyltransferase (ChAT) immunohistochemistry along with the electromyographic (EMG) recordings of denervation-induced fibrillation activity. The results indicate that following PNI, the nNOS immunoreactivity was significantly increased in lesioned neurons peaking at 14 days. The up-regulation of nNOS temporally coincided with the reduction of ChAT and SOD in which the Cu/Zn-SOD showed a greater diminution than Mn-SOD. However, following melatonin administration, the nNOS augmentation was successfully suppressed and the activities of Mn-SOD, Cu/Zn-SOD, and ChAT were effectively preserved at all postaxotomy periods. EMG data also showed a decreased fibrillation in melatonin-treated groups, suggesting a potential effect of melatonin in promoting functional recovery. In association with its significant capacity in preserving SOD reactivity, melatonin is suggested to serve as a powerful therapeutic agent for treating PNI-relevant oxidative damage.

AB - Peripheral nerve injury (PNI) produces functional changes in lesioned neurons in which oxidative stress is considered to be the main cause of neuronal damage. As superoxide dismutase (SOD) is an important antioxidative enzyme involved in redox regulation of oxidative stress, the present study determined whether melatonin would exert its beneficial effects by preserving the SOD reactivity following PNI. Adult rats subjected to hypoglossal nerve transection were intraperitoneally injected with melatonin at ones for 3, 7, 14, 30 and 60 days successively. The potential neuroprotective effects of melatonin were quantitatively demonstrated by neuronal nitric oxide synthase (nNOS), mitochondrial manganese SOD (Mn-SOD), and cytosolic copper-zinc SOD (Cu/Zn-SOD) immunohistochemistry. The functional recovery of the lesioned neurons was evaluated by choline acetyltransferase (ChAT) immunohistochemistry along with the electromyographic (EMG) recordings of denervation-induced fibrillation activity. The results indicate that following PNI, the nNOS immunoreactivity was significantly increased in lesioned neurons peaking at 14 days. The up-regulation of nNOS temporally coincided with the reduction of ChAT and SOD in which the Cu/Zn-SOD showed a greater diminution than Mn-SOD. However, following melatonin administration, the nNOS augmentation was successfully suppressed and the activities of Mn-SOD, Cu/Zn-SOD, and ChAT were effectively preserved at all postaxotomy periods. EMG data also showed a decreased fibrillation in melatonin-treated groups, suggesting a potential effect of melatonin in promoting functional recovery. In association with its significant capacity in preserving SOD reactivity, melatonin is suggested to serve as a powerful therapeutic agent for treating PNI-relevant oxidative damage.

KW - Functional recovery

KW - Hypoglossal nucleus

KW - Melatonin

KW - Nitric oxide

KW - Peripheral nerve injury

KW - Quantitative image analysis

KW - Superoxide dismutase

UR - http://www.scopus.com/inward/record.url?scp=39149142496&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=39149142496&partnerID=8YFLogxK

U2 - 10.1111/j.1600-079X.2007.00505.x

DO - 10.1111/j.1600-079X.2007.00505.x

M3 - Article

VL - 44

SP - 172

EP - 180

JO - Journal of Pineal Research

JF - Journal of Pineal Research

SN - 0742-3098

IS - 2

ER -