ABSTRACT
Objective To evaluate the effect of sevoflurane on cognitive function of mice with Alzheimer's disease.Methods Twenty male mice carrying mnutations in amyloid precusor protein (APP) and presenilin 1 genes,weighing 30-40 g,aged 7 months,were divided into either sevoflurane group (group Sev) or control group (group C),with 20 mice in each group.Mice inhaled 3％ sevoflurane for 4 h in group Sev,and mice inhaled 30％ oxygen for 4 h in group C.At 1 month after inhaling sevoflurane or oxygen,the mice underwent continuous multiple-trail inhibitory avoidance training.The mice were then sacrificed and hippocampi were isolated for determination of the number of Aβ plaques (by immunohistochemistry) and expression of APP and Tau (S396) phosphorylation (by Western blot).Results Compared with group C,the memory lateucy was significantly shortened,the number of Aβ plaques was increased,the phosphorylation of Tau (S396) was increased,and the expression of APP was up-regulated in group Sev (P＜0.05).Conclusion Sevoflurane can decrease the cognitive function of mice with Alzheimer's disease.
ABSTRACT
The effective therapeutics for the sinoatrial node (SAN) pacemaker dysfunction induced by SCN5A gene mutation this is still being explored recently. In this study, a two-dimensional experimental model of rabbit SAN-atrial cell system which proposed by Zhang et al., was used as a prototype, the gene mutation was considered, and effects of both the acid concentration and temperature were also introduced. The effects of acid concentration and temperature on sick sinus syndrome (SSS) at the tissue level were investigated by simulation. The results showed that the SAN abnormal pacemaker could be caused by the reduction of I(Na), which is induced by the two mutations of T220I and delF1617. The results also showed that if we properly adjusted the acid concentration and temperature of the system, not only could we increase the relevant currents, but also could we increase I(Na) which reduced by gene mutations, so that the pacemaking behavior of SAN tissue could return to normal state from abnormalities. The above simulation results imply that the abnormal pacemaking of SAN system may closely relate to the gene mutation of ion channel mutations, and the acid concentration and temperature may play a modulatory role. Our study could be useful for clinical medical diagnosis and therapy of cardiac disease.