Effect of endogenous sulfur dioxide on spatial learning and memory and hippocampal damages in the experimental model of chronic cerebral hypoperfusion

Abstract

BackgroundThe vascular changes due to cerebrovascular damage, especially on the capillaries, play a vital role in causing vascular dementia. Increasing oxidative stress can lead to tissue damage while reducing brain blood flow. The use of factors reducing the oxidative stress level can decrease the brain damages. Sulfur dioxide (SO2) is one of the most important air pollutants that lead to the development of severe brain damage in large quantities. However, studies have recently confirmed the protective effect of SO2 in cardiac ischemic injury, atherosclerosis and pulmonary infections.MethodsThe permanent bilateral common carotid artery occlusion (BCAO) method was used to induce chronic cerebral hypoperfusion (CCH). Two treatment groups of SO2 were studied. The animal cognitive performance was evaluated using the Morris water maze. Hippocampal tissue damage was examined after 2 months of BCAO. In the biochemical analysis, the activity of catalase and lipid peroxidation of the hippocampus was studied.ResultsNeuronal damage in hippocampus, as well as cognitive impairment in ischemia groups treated with SO2 showed a significant improvement. Catalase activity was also significantly increased in the hippocampus of treated groups.ConclusionsAccording to the results, SO2 is likely to be effective in reducing the CCH-caused damages by increasing the antioxidant capacity of the hippocampus.

The Chinese herb Fructus Broussonetiae aids learning and memory in chronic cerebral hypoperfusion by reducing proinflammatory microglia activation in rats

“…Chronic cerebral hypoperfusion is a pathological state involved in the generation of dementia. Consistent with the previous study (Choi et al, 2016), spatial learning and memory impairment testing by the Morris water maze is observed in our model of CCH (Ghasemi et al, 2020). We proved for the first time that Fructus Broussonetiae could improve long-term memory revealed by increased frequency of platform crossing and shortened escape latency time.…”

Small Vessel Disease-Related Dementia: An Invalid Neurovascular Coupling?

“…Other experiments demonstrated that the selective alpha-7-nicotinic AChR antagonism exacerbates the hypoxic effects on the CA1 and CA3 cortical areas; on the contrary, non-selective nicotinic AChR antagonists have a detrimental effect on the hippocampus, not in all the other cortical areas [158][159][160][161]. The chronic reduction of the cerebral blood flow can affect the control of the cholinergic networks, but it happens that a proper cholinergic function is compulsory to well-regulation of the regional brain blood flow [162,163]. Ach principally mediates the parasympathetic innervation of the Willis circle and the pial vessels [164].…”

Different components of air pollutants and neurological disorders

“…Another study found that the combined effect of SO 2 and PM 2.5 led to the accumulation of Aβ in the cerebral cortex and hippocampus of rats ( 28 ). However, other studies have found that SO 2 may alleviate the injury caused by chronic cerebral hypoperfusion by enhancing the antioxidant capacity of the hippocampus ( 29 ). In addition, it has been reported that low doses of PM 2.5 and SO 2 coexposure can lead to neurodegenerative changes, including neuronal apoptosis and reductions in synaptic structural and functional proteins ( 30 ).…”