Microstructural, Immunoreactivity and Biochemical Studies of the Cerebellum after Artequin Administration in Adult Wistar Rats

Abstract

Aims: Artequin (ATQ) is a combination therapy antimalarial drug. Its effects on the microstructural, immunoreactivity and biochemical parameters were investigated in the cerebellum of adult Wistar rats. Study Design: Forty-two inbred adult male Wistar rats of average weight 200 g were divided into groups 1–6. Group 1 served as the control that received 5 ml kg-1 of water, while groups 2–6 received oral doses of 0.86/1.07 mg kg-1 (ATQ1), 1.71/2.14 mg kg-1 (ATQ2), 3.42/4.28 mg kg-1 (ATQ3), 6.84/8.56 mg kg-1 (ATQ4) and 13.68/17.12 mg kg-1 (ATQ5) body weight of artequin for three days Place and Duration of Study: This research took place at the Department of Zoology, Faculty of Biological Sciences, Akwa Ibom State University, Nigeria and Department of Anatomy, Faculty of Basic Medical Sciences, University of Uyo, Akwa Ibom State, Nigeria, between June 2024 and July 2024. Methodology: The animals were sacrificed after they were deeply anesthetized with ketamine–hydrochloride. Biochemical assays for oxidative stress were carried out for superoxide dismutase, malondialdehyde and catalase. The brains were perfused fixed in 10 % buffered formalin. They were processed using haematoxylin and eosin, Bielschowsky silver impregnation and immunohistochemical labelling for glial fibrillary acidic proteins. Results: There was a high significant difference (P = .05) in serum concentration of malondialdehyde in ATQ5 when compared to the control and the other treatment groups; there was no significant difference in superoxide dismutase and catalase between the artequin groups and the control group. The cerebellum of the ATQ groups showed histopathological features including cell atrophy, pyknosis, karyorrhexis, hypertrophy and decreased (P = .05) cellular densities, with increased expressions of glial fibrillary acidic proteins when compared with the control group. Conclusion: Artequin administration induced a dose-dependent adverse effects on the microstructure and GFAP immunolabelling of the cerebellum. This may suggest neuronal and glial degeneration, thus resulting in altered cerebellar functions