Effect of dietary ginger (Zingiber officinale) on the memory and hippocampal neuronal count of cigartte smoke-exposed mice (Mus musculus).

Abstract

Secondhand smoke from cigarettes contains reactive oxygen species which can cause oxidative stress when inhaled. Dietary enrichment with antioxidants can help mitigate oxidative stress, thereby reducing brain damage and probably improving cognitive function. In the present study, the neuroprotective effect of dietary ginger (Zingiber officinale) against oxidative stress caused by cigarette smoking was tested. The test subjects were divided into four groups and were treated as follows: Group 1 and Group 2 mice were not given any supplementation; Group 3 mice were supplemented with 0.25 g vitamin C per kg body weight and Group 4 mice were supplemented with 0.1 g ginger extract per kg body weight. All mice except Group 1 were then exposed to cigarette smoke in an improvised smoke chamber for 15 minutes per day for a period of 10 days. The Morris water maze (MWM) test was administered to test mice before supplementation, during supplementation and after smoke exposure to assess memory-related skills. The density of neurons in the hippocampus was measured histologically via a modified planimetric method. Linear regression analysis was used to test if there is a relationship between cognitive ability and neuron density. Results indicate that the ginger extract has no apparent memory enhancing ability. Both the ginger extract and vitamin C did not show any ability to increase neuron density. Linear regression analysis of the Group 2 mice revealed that cognitive ability and neuron density have a negative correlation. These results may be attributed to the selective property of the blood brain barrier and the adequate defenses of the brain against inhaled contaminants on normal test subjects. However, the mitigating effects of dietary ginger may be more apparent in test animals subjected to invasive procedures than in intact individuals. The implications of the findings with regard to the disruption of synaptic connections due to cigarette smoke exposure during cognitive development are discussed.