open access

Vol 82, No 1 (2023)
Original article
Submitted: 2021-07-31
Accepted: 2021-12-29
Published online: 2022-01-17
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Vitamin D3 promotes oligodendrogenesis and modulates synucleinopathy in lead-induced nigral pars compacta neurotoxicity in rats

R. A. Imam1, M. R. Abdel-Hamed2
·
Pubmed: 35099046
·
Folia Morphol 2023;82(1):42-52.
Affiliations
  1. Department of Anatomy and Embryology, Faculty of Medicine, Cairo University, Egypt
  2. Department of Anatomy and Embryology, Faculty of Medicine, Ain Shams University, Egypt

open access

Vol 82, No 1 (2023)
ORIGINAL ARTICLES
Submitted: 2021-07-31
Accepted: 2021-12-29
Published online: 2022-01-17

Abstract

Background: Lead-induced neurotoxicity was marked with locomotor and Parkinsonian-like changes. Oligodendrocytes and synucleinopathy were signed to in the pathophysiology of some neurodegenerative diseases. Vitamin D3’s (D3) role in substantia nigra pars compacta (SNpc) disorders is debated between neuroscientists. The aim of the study was to investigate lead-induced SNpc neurotoxic changes and explore the possible neuroprotective role of D3 and the possible involvement of oligodendrocytes and α-synuclein.
Materials and methods: This study included 40 adult Wistar rats assigned into four equal groups: control, lead (Pb) (in drinking water, 1,000 mg/L), Pb + D3 (D3 injection, 1,000 IU/kg IM; 3 days/week), and D3. After 8 weeks, the rats were sacrificed, and their midbrain underwent biochemical and immunoblotting analysis. Midbrain paraffin blocks were stained for histological and immunohistochemical assessment.
Results: Lead (Pb) had increased significantly (p < 0.05) nigral α-synuclein and caspase-11 by immunoblotting analysis. Histologically, it induced neurodegeneration in SNpc and significantly decreased neuronal cell density by cresyl violet staining. Pb also significantly reduced SNpc tyrosine hydroxylase immunoreaction, significantly elevated glial fibrillatory acid protein (GFAP) and α-synuclein immunoreaction associated with a mild but significant increase in caspase-3. In the Pb + D3 group, all the previous deleterious changes were significantly alleviated in addition to significant upregulation of anti-oligodendrocytes immunoexpression.
Conclusions: Lead (Pb) may induce SNpc neurotoxicity presumably via activation of caspase-11 and α-synuclein. D3 may modulate this neurotoxicity probably through an oligodendrogenic effect.

Abstract

Background: Lead-induced neurotoxicity was marked with locomotor and Parkinsonian-like changes. Oligodendrocytes and synucleinopathy were signed to in the pathophysiology of some neurodegenerative diseases. Vitamin D3’s (D3) role in substantia nigra pars compacta (SNpc) disorders is debated between neuroscientists. The aim of the study was to investigate lead-induced SNpc neurotoxic changes and explore the possible neuroprotective role of D3 and the possible involvement of oligodendrocytes and α-synuclein.
Materials and methods: This study included 40 adult Wistar rats assigned into four equal groups: control, lead (Pb) (in drinking water, 1,000 mg/L), Pb + D3 (D3 injection, 1,000 IU/kg IM; 3 days/week), and D3. After 8 weeks, the rats were sacrificed, and their midbrain underwent biochemical and immunoblotting analysis. Midbrain paraffin blocks were stained for histological and immunohistochemical assessment.
Results: Lead (Pb) had increased significantly (p < 0.05) nigral α-synuclein and caspase-11 by immunoblotting analysis. Histologically, it induced neurodegeneration in SNpc and significantly decreased neuronal cell density by cresyl violet staining. Pb also significantly reduced SNpc tyrosine hydroxylase immunoreaction, significantly elevated glial fibrillatory acid protein (GFAP) and α-synuclein immunoreaction associated with a mild but significant increase in caspase-3. In the Pb + D3 group, all the previous deleterious changes were significantly alleviated in addition to significant upregulation of anti-oligodendrocytes immunoexpression.
Conclusions: Lead (Pb) may induce SNpc neurotoxicity presumably via activation of caspase-11 and α-synuclein. D3 may modulate this neurotoxicity probably through an oligodendrogenic effect.

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Keywords

lead (Pb), pars compacta, D3-synucleiopathy, oligodendrocytes

About this article
Title

Vitamin D3 promotes oligodendrogenesis and modulates synucleinopathy in lead-induced nigral pars compacta neurotoxicity in rats

Journal

Folia Morphologica

Issue

Vol 82, No 1 (2023)

Article type

Original article

Pages

42-52

Published online

2022-01-17

Page views

3427

Article views/downloads

951

DOI

10.5603/FM.a2022.0003

Pubmed

35099046

Bibliographic record

Folia Morphol 2023;82(1):42-52.

Keywords

lead (Pb)
pars compacta
D3-synucleiopathy
oligodendrocytes

Authors

R. A. Imam
M. R. Abdel-Hamed

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