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Biography

Saliha Aysenur Cam has completed his Graduation from Hacettepe University, Faculty of Pharmacy. He is pursuing his PhD in Pharmacology Department at Ankara
Yildirim Beyazit University. He currently works as a Lecturer at Ankara Yildirim Beyazit University. His primary area of interest is neuropharmacology.

Abstract

Alzheimer’s disease (AD) currently is one of the major healthcare issues worldwide. Unfortunately current therapies for
Alzheimer’s disease do not modify the course of disease. Nigella sativa and its active constituent Th ymoquinone (TQ) may
have anti-neuro=-infl ammatory actions. Th e aim of the present study was to investigate possible protective eff ects of Nigella
sativa oil (NSO) and TQ on Aβ42-induced AD models of rats. Intrahippocampal injection of Aβ42 peptide provides glial cell
responses and causes neuro-infl ammation. NSO and TQ were orally administered daily for 7 days before and for 10 days
aft er bilateral intrahippocampal Aβ injection. To investigate whether NSO or TQ improve cognition, Passive Avoidance (PA)
and Morris Water Maze (MWM) behavioral tests were performed 10 days later Aβ injection to asses learning and memory
of rats. Aft er the probe test the brain tissues were collected. Immunohistochemical staining with Iba1, GFAP and Caspase-3
antibody and ELISA analysis of TNF-α and IL-1β levels on hippocampal tissue were performed. Th e oral treatment with
NSO or TQ signifi cantly reduced cognitive impairments in behavioral tests both MWM and PA. Immuno-staining results
revealed that both NSO and TQ reduced microglial and astrocytic activation increased with Aβ injection. Measurements of
pro-infl ammatory cytokines in hippocampal tissue of Aβ-injected rats showed an elevation of TNF-α and IL-1β levels. Th ese
changes were signifi cantly reversed by NSO and TQ treatment. In conclusion results represent that NSO and TQ can improve
Aβ-induced cognitive impairments by inhibiting neuro-infl ammation. NSO and TQ recommended as a candidate for further
investigation in treatment of AD.