Abstract:

Aim: Chronic cerebral hypoperfusion (CCH) leads to vascular dementia with progressive hippocampal damage and cognitive impairments. CCH also causes a decrease in blood flow in the retina.The aim of this study was to investigate the effects of spironolactone on oxidative stress and glycogen levels in the eye and prefrontal cortex (PFC) tissues in ovariectomized rats with CCH. Material and Methods: 32 female Wistar Albino rats were randomly divided into 4 groups, 8 in each group: 1)Control, 2)KSH, 3) KSH+Spironolactone 25mg/kg 4)KSH+Spironolactone 50mg/kg. The rats underwent bilateral ovariectomy (OVX) at the start of the experiment, a CCH model was created with permanent occlusion of the common carotid arteries (2VO) 5 weeks after OVX. Spironolactone was administered by oral gavage three days before 2VO and once daily for 3 weeks after 2VO. At the end of the experiment, tissue glycogen, reduced glutathione (GSH), malondialdehyde (MDA) and ascorbic acid (AA) levels were measured. Statistical analysis was performed using ANOVA and Bonferroni tests. Results: CCH caused an increase in oxidative stress markers and a decrease in glycogen level in PFC. Similarly, CCH caused a decrease in both glycogen and AA levels in the eye tissue. In the group treated with 25mg/kg spironolactone, the AA and PFC glycogen levels of the eyes decreased, while the MDA levels in the PFC were increased compared to the CCH group(p<0.05). In the group administered 50mg/kg spironolactone, PFC glycogen levels and eye glycogen levels were significantly increased compared to the CCH group(p<0.05). Conclusion: Our results show that spironolactone administration can be effective in reducing retinal and cerebral damage caused by CCH by reducing oxidative stress and increasing glycogen levels in PFC and eye tissues in ovariectomized rats with CCH

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