Pakeer Oothuman

Improved spatial learning and memory performance following Tualang honey treatment during cerebral hypoperfusion-induced neurodegeneration

Honey has shown potential therapeutic properties in traditional medicine. This study investigated the cognition enhancing potential of Tualang honey in chronic cerebral hypoperfusion- induced neurodegeneration by permanent bilateral common carotid arteries ligation (2 vessels occlusion- 2VO) in rats. Previous studies have shown that rats subjected to 2VO (2 vessel occlusion) experienced cognitive deficits, oxidative stress and neuronal injury in the hippocampus of the brain. We studied the effect of Tualang honey on learning and memory using the Morris water maze (MWM) in rats. Rats were randomly divided into four groups (n=10); Sham control, untreated 2VO (2VO), honey treated 2VO (2VO+H) and honey treated group (H). Each group was again divided into two subgroups (n=5): one for long term memory assessment and another for short term memory and relearning tasks. After 10 weeks of treatment, all rat groups were tested for cognitive assessment by MWM (Morris water maze). 2VO+H rats had better spatial learning and memory performance than untreated 2VO rats in MWM tasks (p 0.05). This study shows that Malaysian Tualang honey might have therapeutic potential for the treatment of chronic cerebral hypoperfusion related neurodegenerative disorders such as Alzheimer’s disease (AD) in which cognitive impairment is profound.

Oxidative Stress Status and Neuroprotection of Tocotrienols in Chronic Cerebral Hypoperfusion-Induced Neurodegeneration Rat Animal Model

Background: Reduced cerebral blood flow is associated with aging, neurodegenerative disorders, and an increased formation of reactive oxygen species. This study was designed to assess the potential use of vitamin E as an antioxidant and neuroprotective agent using 2-vessel occlusion (2VO) rat animal model. Materials and Methods: Twenty-four Sprague Dawley rats weighing 200–250 g were equally divided into the following three groups: SHAM control, 2VO, and 2VO+E (treated daily with vitamin E tocotrienol, 100 mg/kg, orally following 2VO). On the 8th week after 2VO surgery, rats were euthanized and the hippocampi were isolated with the estimation of viable neuronal cell count in the hippocampal CA-1 region. The isoprostane F2 (Iso-F2) levels were also measured in the brain homogenates to quantify the oxidative stress levels. Results: There was significantly higher neuronal cell death in the hippocampal CA-1 region and increased Iso-F2 levels in the 2VO group compared to the SHAM control group (P < 0.05). Conversely, no significant difference was observed with regard to the neuronal cell death and Iso-F2 levels in the 2VO+E group and the SHAM control group (P > 0.05). Conclusion: This study demonstrates the effectiveness of vitamin E tocotrienol as a neuroprotective and antioxidant agent in chronic cerebral hypoperfusion-induced neurodegeneration in rats.