EFFECT OF KHAYA SENEGALENSIS CARDIAC GLYCOSIDE ON EXPRESSION SIGNATURE (IBA-1) IN PREFRONTAL CORTEX OF ISCHEMIC STROKE RAT MODEL
Abstract
ABSTRACT
Amitriptyline like many other antidepressant medications plays a central role in managing mood disorders, providing crucial support to individuals grappling with conditions such as depression and anxiety.. This study aims to investigate the effects of Khaya senegalensis cardiac glycoside on expression signature (Iba-1) in the prefrontal cortex following amitriptyline induced ischemic stroke in wistar rats. A total of eighty healthy male Wistar rats weighing 160-208g were grouped into 11 groups (n = 6): The experiment was divided in 2 phases, phase I: stroke induction, using a single dose of 1.2 mg/kg of AMT for 3 days. Phase II: treatment groups, the rats were subdivided into AMT group (stroke rats), left untreated and 3 treatment groups, which were treated with KS orally, at doses of 200, 300 and 400mg/kg body weight, designated as COMLD + AMT, COMMD + AMT and COMHD + AMT respectively, for a period of two weeks. Control was administered with distilled water. After administration the rats were euthanized using cervical dislocation and the brain were collected and fixed in 10% neutral buffered formalin for Immunohistochemical (IHC) for IBA1 using ImmPRESS™ Immunohistochemical Detection. Ionized calcium-binding adaptor molecule 1 (IBA-1) immunoreactive microglial cells were weakly stained in the control rats. The number of immunoreactive microglial cells thickly stained and there was increase in number of cells in AMT treated rats compared to control. The number of reactive microglial reduced when treated with COM KSC.GLY+AMT (LD; 200 mg/kg + AMT), KSC.GLY+AMT (SD; 300 mg/kg + AMT) and KSC.GLY+AMT (HD; 400 mg/kg + AMT). Reduction in number of reactive microglial was observed higher in group KSC.GLY+AMT (LD; 200 mg/kg + AMT) and KSC.GLY+AMT (SD; 300 mg/kg + AMT) compared to KSC.GLY+AMT (HD; 400 mg/kg + AMT) plates. This study suggests that Khaya senegalensis cardiac glycoside can attenuate cortical microglial activation in AMT-induced ischemic stroke rat model.
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