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1.
Journal of Central South University(Medical Sciences) ; (12): 641-647, 2023.
Article in English | WPRIM | ID: wpr-982333

ABSTRACT

OBJECTIVES@#Application of ultrashort wave (USW) to rats with cerebral ischemia and reperfusion injury could inhibit the decrease of expression of secretory pathway Ca2+-ATPase 1 (SPCA1), an important participant in Golgi stress, reduce the damage of Golgi apparatus and the apoptosis of neuronal cells, thereby alleviating cerebral ischemia-reperfusion injury. This study aims to investigate the effect of USW on oxygen-glucose deprivation/reperfusion (OGD/R) injury and the expression of SPCA1 at the cellular level.@*METHODS@#N2a cells were randomly divided into a control (Con) group, an OGD/R group, and an USW group. The cells in the Con group were cultured without exposure to OGD. The cells in the OGD/R group were treated with OGD/R. The cells in the USW group were treated with USW after OGD/R. Cell morphology was observed under the inverted phase-contrast optical microscope, cell activity was detected by cell counting kit-8 (CCK-8), apoptosis was detected by flow cytometry, and SPCA1 expression was detected by Western blotting.@*RESULTS@#Most of the cells in the Con group showed spindle shape with a clear outline and good adhesion. In the OGD/R group, cells were wrinkled, with blurred outline, poor adhesion, and lots of suspended dead cells appeared; compared with the OGD/R group, the cell morphology and adherence were improved, with clearer outlines and fewer dead cells in the USW group. Compared with the Con group, the OGD/R group showed decreased cell activity, increased apoptotic rate, and down-regulating SPCA1 expression with significant differences (all P<0.001); compared with the OGD/R group, the USW group showed increased cell activity, decreased apoptotic rate, and up-regulating SPCA1 expression with significant differences (P<0.01 or P<0.001).@*CONCLUSIONS@#USW alleviates the injury of cellular OGD/R, and its protective effect may be related to its up-regulation of SPCA1 expression.


Subject(s)
Animals , Rats , Apoptosis , Brain Ischemia , Glucose/metabolism , Oxygen/metabolism , Reperfusion Injury/metabolism , Transcriptional Activation , Up-Regulation , Calcium-Transporting ATPases/metabolism
2.
Chinese Journal of Physical Medicine and Rehabilitation ; (12): 11-14, 2018.
Article in Chinese | WPRIM | ID: wpr-711264

ABSTRACT

Objective To observe the influence of ultra-shortwave (USW) irradiation on infarct volume and Ca2+-ATPase (SPCA) secretion after brain ischemia and reperfusion.Methods Eighty Sprague-Dawley rats were randomly divided into a sham operation group (n=8),a model group (n=36) and a USW group (n=36).The animal model of middle cerebral artery ischemia and reperfusion (MCAO/R) was established using the suture method in the rats of the model and USW groups,while the sham operation group was given the same operation but without inserting the thread plug.One day,3 days and 7 days after the intervention,12 rats were sacrificed and the infarct volumes and SPCA1 protein expression were measured using 2,3,5-triphenyltetrazolium chloride staining and western blotting.Results No white infarcted tissue was found in the sham operation group.In the model and USW groups the volume of infarcted tissue decreased with time.Significantly less infarcted volume was observed in the USW group compared to the model group at each time point.The SPCA1 levels in the brain tissue were lower than in the sham operation group after one and 3 days of USW treatment,but they were significantly lower in the model group as well.As time went by,the average SPCA1 level increased significantly in the model and USW groups.A slightly higher SPCA1 level was observed in the USW group compared to the model group after one day of treatment,but with no significance.However,significant differences were found between them after 3 and 7 days of intervention.Conclusion Ultra-shortwave irradiation can protect against MCAO/R injury by decreasing the infarcted volume,which may be related to down-regulation of SPCA1,minimizing nerve cell apoptosis and promoting neural functional recovery,at least in rats.

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