Adjuvant Protective Effect of Melatonin against Diabetogenic Structural Changes of Alloxan on Adult Albino Rats Cerebellar Cortex

Document Type : Original Article

Authors

1 Department of Anatomy & Embryology, Faculty of Medicine, Ain Shams University, Cairo, Egypt. Department of Anatomy, Histology, Physiology and Biochemistry, Faculty of Medicine, The Hashemite University, Zarqa, Jordan.

2 Department of Anatomy & Embryology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

3 Department of Anatomy & Embryology, Faculty of Medicine, Ain Shams University, Cairo, Egypt

4 Department of Anatomy & Embryology, Faculty of Medicine, Ain Shams University, Cairo, Egypt. Department of Anatomy, Faculty of Medicine, Hail University, KSA.

Abstract

Background: A prevalent metabolic disease with well-known, dangerous secondary consequences is diabetes mellitus. Damage to the central nervous system is also linked to it. The impairment of cerebellar functioning together with histochemical and structural abnormalities are characteristics of this injury. Aim of the study: Was to determine how the adult albino rats’ cerebellum histological structure was affected by diabetes mellitus brought on by alloxan as well as any potential preventive effects of melatonin taken orally against the rats’ cerebellar structural damage. Material and methods: Throughout the course of the investigation, four equal groups of twenty-four adult albino rats were formed at random. The control group was Group I, while the diabetic group was group II , which received one alloxan injection at a 150 mg/ kg/ b.w. dosage, Group III (the positive control group) consumed melatonin orally at a dose of 10 mg/kg/b.w. daily for four weeks, and Group IV (the diabetic group treated with melatonin) received oral melatonin at a dose of 10 mg/ kg/ b.w. daily for four weeks following the induction of diabetes by alloxan monohydrate intraperitoneal in a dose of 150 mg/ kg/b.w. Cerebella samples were obtained, prepared into paraffin blocks, and examined under a light microscope after a month. Results: In group II, the cerebellar cortex showed signs of degeneration, particularly in the Purkinje cell layer. Strong evidence of gliosis was present, validated by an elevated level in the astrocyte count. In group IV there was an alleviation of the cerebellar morphology following melatonin treatment. Melatonin improved cerebellar thickness, reduced the quantity of astrocytes while regaining Purkinje cell number and morphology. Conclusion: The melatonin plays a role in the protection of the cerebellum from diabetic-induced neuronal damage.

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