New insight on the role of Granulocyte Colony Stimulating Factor in protecting cerebellar cortex against Aluminum Chloride induced cytotoxicity via improving cell survival and reducing neuroinflammation in albino rats

Articles in Press

Document Type : Original Article

Authors

1 Department of Histology and Cell Biology, Faculty of Medicine, Benha University, Egypt.

2 Department of Clinical Pharmacology, Faculty of Medicine, Benha University, Egypt.

3 Department of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Benha University, Egypt.

Abstract

Background: Aluminum (Al) is a potent neurotoxin that contributes to a wide range of neurodegenerative and neurodevelopmental disorders in both humans and animals. Granulocyte colony-stimulating factor (G-CSF) can be a promising protective drug.
Aim of the study: Assessment of the neuroprotective potential of G-CSF on the aluminum chloride (AlCl3)-induced cerebellar cortex toxicity in rats.
Material and methods: A total of thirty-six adult male albino rats were used in this study. The rats were divided into three equal groups; group I (control group): rats were divided into 3 subgroups, group II (AlCl3 group): rats received AlCl3 at a dose of (100 mg/kg/day) by oral gavage intragastrically for 21 days, group III (G-CSF +AlCl3 group): rats received aluminum chloride (AlCl3) as in group II for 21 days, and were injected subcutaneously with G-CSF (100 µg/kg/day) for five days before AlCl3 and continued for another 21 days with AlCl3. G-CSF was injected 30 minutes before AlCl3. After perfusion fixation process, skulls were opened and the cerebellar cortex specimens were immediately processed for light and electron microscopic examination.
Results: The results of this study lead to the conclusion that G-CSF protects the cerebellar cortex. The histological observations showed that group II revealed extensive neuro-degeneration of the cerebellar cortex. Calbindin immunoreactivity showed a significant decrease (P < 0.05) in Purkinje cells, while Bax and TNF-α immunoreactivity showed a significant increase (P < 0.05) in all layers of cerebellar cortex compared to group I. G-CSF pre-treatment in group III enhanced all these histological and statistical parameters.
Conclusion: The results of this study lead to the conclusion that G-CSF protects the cerebellar cortex against AlCl3-induced neurotoxicity. This neuroprotective effect is mediated by its anti-inflammatory and anti-apoptotic effects.

Keywords

Egyptian Journal of Histology

Articles in Press, Accepted Manuscript
Available Online from 07 September 2022

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