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 | ||||
| Egyptian Journal of Histology | ||||
| Articles in Press, Accepted Manuscript, Available Online from 07 September 2022 | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/ejh.2022.148618.1718 | ||||
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| Authors | ||||
Heba Bayoumi  1; Enas Shaban2; Shaymaa Haroun2; Marwa Mohamed Morad3; Enas Elgendy1
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| 1Department of Histology and Cell Biology, Faculty of Medicine, Benha University, Egypt. | ||||
| 2Department of Clinical Pharmacology, Faculty of Medicine, Benha University, Egypt. | ||||
| 3Department 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 | ||||
| Keywords: Cerebellar cortex; Aluminum chloride; G-CSF; neurotoxicity | ||||
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