Therapeutic Response of Sulforaphane on Oxidative Stress and Cognitive Impairment in Aluminum-Induced Alzheimer-type Hippocampal Neurodegeneration in Adult Wistar Rats

The accumulation of Aluminum in the brain is believed to be involved in the pathophysiology of neurodegenerative diseases including Alzheimer’s disease. This study evaluated the neuroprotective activities of sulforaphane (SFN) on aluminum chloride (AlCl3)-induced hippocampal degeneration in Wistar rats. A total of 28 adult male Wistar rats were divided into four groups (n=7). Group A (control) received 200 mg/kg of normal saline solution ad libitum; Group B received 200 mg/kg body weight of AlCl3; Group C received 200 mg/kg of SFN and 200 mg/kg of AlCl3; Group D received 200 mg/kg of SFN alone. All administrations were done daily, through oral gavage for 45 days and the rats underwent behavioral tests such as Y-maze and Open field test. On day 46, blood samples were collected to obtain serum for analysis and the brains were harvested for assessment. The results showed significant memory decline, spatial memory impairment and learning deficit, decreased levels of oxidative markers with corresponding increase in stress markers among AlCl3 only group compared to control but was attenuated with SFN administration. There were also significant differences in the levels of neurotransmitters in SFN and AlCl3 before and after treatment with SFN. Histological examination revealed clear pathological alterations indicative of hippocampal degeneration, including distortion and pyknotic abnormalities in the pyramidal layer of the AlCl3-only group's hippocampal region, which were mitigated by SFN treatment. SFN improved learning and memory, antioxidant enzymes, neurotransmitters, and morphology of hippocampus thereby attenuating the neurotoxic effects of AlCl3.

Key Words: Alzheimer’s disease, aluminum chloride, behavioural stress test, hippocampus, oxidative stress.