Hypothyroid state does not protect but delays neuronal death in the hippocampal CA1 region following transient cerebral ischemia

Focus on oxidative stress and gliosis

Choong Hyun Lee, Ki Yeon Yoo, In Koo Hwang, Jung Hoon Choi, Ok Kyu Park, Hua Li, Il Jun Kang, Young-Guen Kwon, Young Myeong Kim, Moo Ho Won

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

We investigated protective effects of hypothyroidism on delayed neuronal death, gliosis, lipid peroxidation and Cu,Zn-superoxide dismutase (SOD1) in the gerbil hippocampal CA1 region (CA1) after 5 min of transient cerebral ischemia. The hypothyroidism was induced by 0.025% methimazole treatment. Free triiodothyronine and thyroxine levels were markedly decreased in the hypothyroid group. Four days after ischemia/reperfusion, only a few NeuN-immunoreactive (+) neurons were detected in the CA1 of euthyroid-ischemia (eu-ischemia) group; however, at this time point, the number of NeuN+ neurons was significantly higher in the hypothyroid-ischemia (hypo-ischemia) group than in the eu-ischemia group. At 5 days postischemia, NeuN+ neurons were significantly decreased in the hypo-ischemia group: The number of NeuN + neurons in this group was similar to that in the eu-ischemia group. Activations of GFAP+ astrocytes and Iba-1+ microglia in the CA1 were higher in the eu-ischemia group 3 and 4 days after ischemia/reperfusion. At 5 days postischemia, the activations of both the glial cells in the CA1 were similar between the two groups. 4-Hydroxy-2-nonenal (HNE), a marker for lipid peroxidation, immunoreactivity in the eu-ischemia group was higher than in the hypo-ischemia group; at 5 days postischemia, the immunoreactivity was similar between the two groups. In contrast, SOD1 level was lower in the CA1 of the eu-ischemia group. These results suggest that hypothyroid state does not protect against delayed neuronal death but only delays the neuronal death in the hippocampal CA1 region after transient cerebral ischemia by reducing lipid peroxidation and increasing SOD1.

Original languageEnglish
Pages (from-to)2661-2668
Number of pages8
JournalJournal of Neuroscience Research
Volume88
Issue number12
DOIs
Publication statusPublished - 2010 Sep 1

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Hippocampal CA1 Region
Gliosis
Transient Ischemic Attack
Oxidative Stress
Ischemia
Lipid Peroxidation
Neurons
Hypothyroidism
Reperfusion
Methimazole
Gerbillinae
Microglia
Triiodothyronine
Thyroxine
Neuroglia
Astrocytes

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience

Cite this

Lee, Choong Hyun ; Yoo, Ki Yeon ; Hwang, In Koo ; Choi, Jung Hoon ; Park, Ok Kyu ; Li, Hua ; Kang, Il Jun ; Kwon, Young-Guen ; Kim, Young Myeong ; Won, Moo Ho. / Hypothyroid state does not protect but delays neuronal death in the hippocampal CA1 region following transient cerebral ischemia : Focus on oxidative stress and gliosis. In: Journal of Neuroscience Research. 2010 ; Vol. 88, No. 12. pp. 2661-2668.
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abstract = "We investigated protective effects of hypothyroidism on delayed neuronal death, gliosis, lipid peroxidation and Cu,Zn-superoxide dismutase (SOD1) in the gerbil hippocampal CA1 region (CA1) after 5 min of transient cerebral ischemia. The hypothyroidism was induced by 0.025{\%} methimazole treatment. Free triiodothyronine and thyroxine levels were markedly decreased in the hypothyroid group. Four days after ischemia/reperfusion, only a few NeuN-immunoreactive (+) neurons were detected in the CA1 of euthyroid-ischemia (eu-ischemia) group; however, at this time point, the number of NeuN+ neurons was significantly higher in the hypothyroid-ischemia (hypo-ischemia) group than in the eu-ischemia group. At 5 days postischemia, NeuN+ neurons were significantly decreased in the hypo-ischemia group: The number of NeuN + neurons in this group was similar to that in the eu-ischemia group. Activations of GFAP+ astrocytes and Iba-1+ microglia in the CA1 were higher in the eu-ischemia group 3 and 4 days after ischemia/reperfusion. At 5 days postischemia, the activations of both the glial cells in the CA1 were similar between the two groups. 4-Hydroxy-2-nonenal (HNE), a marker for lipid peroxidation, immunoreactivity in the eu-ischemia group was higher than in the hypo-ischemia group; at 5 days postischemia, the immunoreactivity was similar between the two groups. In contrast, SOD1 level was lower in the CA1 of the eu-ischemia group. These results suggest that hypothyroid state does not protect against delayed neuronal death but only delays the neuronal death in the hippocampal CA1 region after transient cerebral ischemia by reducing lipid peroxidation and increasing SOD1.",
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Hypothyroid state does not protect but delays neuronal death in the hippocampal CA1 region following transient cerebral ischemia : Focus on oxidative stress and gliosis. / Lee, Choong Hyun; Yoo, Ki Yeon; Hwang, In Koo; Choi, Jung Hoon; Park, Ok Kyu; Li, Hua; Kang, Il Jun; Kwon, Young-Guen; Kim, Young Myeong; Won, Moo Ho.

In: Journal of Neuroscience Research, Vol. 88, No. 12, 01.09.2010, p. 2661-2668.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Hypothyroid state does not protect but delays neuronal death in the hippocampal CA1 region following transient cerebral ischemia

T2 - Focus on oxidative stress and gliosis

AU - Lee, Choong Hyun

AU - Yoo, Ki Yeon

AU - Hwang, In Koo

AU - Choi, Jung Hoon

AU - Park, Ok Kyu

AU - Li, Hua

AU - Kang, Il Jun

AU - Kwon, Young-Guen

AU - Kim, Young Myeong

AU - Won, Moo Ho

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N2 - We investigated protective effects of hypothyroidism on delayed neuronal death, gliosis, lipid peroxidation and Cu,Zn-superoxide dismutase (SOD1) in the gerbil hippocampal CA1 region (CA1) after 5 min of transient cerebral ischemia. The hypothyroidism was induced by 0.025% methimazole treatment. Free triiodothyronine and thyroxine levels were markedly decreased in the hypothyroid group. Four days after ischemia/reperfusion, only a few NeuN-immunoreactive (+) neurons were detected in the CA1 of euthyroid-ischemia (eu-ischemia) group; however, at this time point, the number of NeuN+ neurons was significantly higher in the hypothyroid-ischemia (hypo-ischemia) group than in the eu-ischemia group. At 5 days postischemia, NeuN+ neurons were significantly decreased in the hypo-ischemia group: The number of NeuN + neurons in this group was similar to that in the eu-ischemia group. Activations of GFAP+ astrocytes and Iba-1+ microglia in the CA1 were higher in the eu-ischemia group 3 and 4 days after ischemia/reperfusion. At 5 days postischemia, the activations of both the glial cells in the CA1 were similar between the two groups. 4-Hydroxy-2-nonenal (HNE), a marker for lipid peroxidation, immunoreactivity in the eu-ischemia group was higher than in the hypo-ischemia group; at 5 days postischemia, the immunoreactivity was similar between the two groups. In contrast, SOD1 level was lower in the CA1 of the eu-ischemia group. These results suggest that hypothyroid state does not protect against delayed neuronal death but only delays the neuronal death in the hippocampal CA1 region after transient cerebral ischemia by reducing lipid peroxidation and increasing SOD1.

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