Cigarette smoking and vascular dementia in rats: Relationships with oxidative stress

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Utkan T. , Yazır Y. , Gacar G. , Göçmez S. S. , Demirtaş Şahin T. , Barış Ö.

31st Congress of the European-College-of-Neuropsychopharmacology (ECNP), Barcelona, Spain, 6 - 09 October 2018, vol.29 identifier


P.161 Cigarette smoking and vascular dementia in rats: Relationships with oxidative stress T. Utkan 1 , ∗, Y. Yazir 2 , G. Gacar 3 , S.S. Gocmez 1 , T. Demirta  ̧s  ̧S ahin 1 , O. Baris 4 1 Kocaeli University Medical Faculty, Department of Phar- macology, Kocaeli, Turkey 2 Kocaeli University Medical Faculty, Department of Histol- ogy and Embryology, Kocaeli, Turkey 3 Kocaeli University, Stem Cell and Gene Theraphy Research and Application Center, Kocaeli, Turkey 4 Kocaeli Derince Education and Research Hospital, Depart- ment of Cardiovascular Surgery, Kocaeli, Turkey Purpose: Chronic exposure to cigarette smoke is consis- tently and causally linked to oxidative stress in animal models. Increased risk of dementia resulting from smok- ing may be realized through cardiovascular disease because smoking-related oxidative stress has been hypothesized as an underlying mechanism for cardiovascular diseases (such as increase in platelet viscosity and endothelial dysfunction) and cardiovascular diseases contribute to an increased risk of vascular dementia. However, few previous studies have reported that smoking may also predispose to vascular de- mentia. Therefore, the present neurobehavioral study was undertaken to evaluate the effect of smoking on cognitive functions, blood pressure, vascular reactivity and oxidative stress in rats. Methods: Eighteen male Wistar rats were divided into two groups, with nine rats in control group, nine rats in the cigarette smoke (smoking) group. The control group were exposed to clean air, while the smoking were exposed to cigarette smoke for 2 h daily with commercially available cigarettes (long LM) for 8 weeks using the modified venti- lated smoking exposure chambers as previously described by Chen et al. After 8-week exposure, passive avoidance (PAT) and Morris water maze test (MWMT) were used for evaluated of cognition. In PAT, preacquisition, acquisition, and reten- tion trials were carried out. In acquisition trial, an electric foot shock (0.5 mA) of a 3s duration was delivered to the an- imal via grid floor. Retention trial was evaluated 24 h post- training by returning the animals into the light compartment and recording their latency to enter the dark compartment. The MWMT was performed in a circular pool and a platform was located at the centre of a fixed quadrant. Rats received three consecutive daily training trials for the following 4 days. On the fifth day, the probe test was performed. The platform was not placed in the pool and the rats were al- lowed to swim freely for 60 s. The total time that subjects spent in the escape platform’s quadrant was recorded. Sys- tolic blood pressure was recorded by tail cuff plethysmog- raphy, their aortas were removed and placed in the organ chambers for isometric tension measurements. Aortas and brains were dissected for ELISA and immunohistochemical analysis. One-way, two-way ANOVA and Kruskal-Wallis tests are used for the statistical analysis. Results: There was no significant difference between two groups for the first day latency while in smoking rats the second day latency was significantly shortened compared to control group in PAT. Also, in MWMT, the results showed a decrease in the time spent in the escape platform’s quadrant in the probe test in smoking rats. Endothelium- dependent vasorelaxation responses and eNOS immunore- activity decreased but endothelium independent vasorelax- ation did not change in smoking rats. No significant change was observed in the systemic blood pressure of animals be- tween two groups. We found that the levels of oxidative stress were significantly increased in the hippocampus of the smoking group. Conclusions: Our data suggested that chronic cigarette smoking could induce cognitive decline, endothelial dys- function and increased oxidative stress in hippocampus. These changes may explain why smoking can predispose brains to vascular dementia