The influence of ultra-shortwave irradiation on Ca2+-ATPase expression after cerebral ischemia and reperfusion / 中华物理医学与康复杂志

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.

Inhibitory Effects of Astragalosides on Proliferation of Lung Adenocarcinoma SPCA-1 Cells / 中国药房

OBJECTIVE:To investigate the inhibitory effect of astragalosides on proliferation of lung adenocarcinoma SPCA-1 cells. METHODS:After the cells were cultured in 0 (blank control),7.8,15.6,31.2,62.5,125.0 and 250.0 μg/ml for 48 h, MTT method was used to determine cell viability and median inhibitory concentration(IC50)was calculated,and terminal deoxynu-cleotidyl transferase-mediated dUTP-biotin nick end labeling assay(TUNEL)and flow cytometry were employed to detect apopto-sis. RESULTS:Compared to the blank control,after the cells were cultured in 7.8,15.6,31.2,62.5,125.0 and 250.0 μg/ml as-tragalosides for 48 h,the cell viability was poorer(P<0.01),and IC50 was 61.75 μg/ml;after the cells were cultured in 15.6,31.2, 62.5,125.0 and 250.0 μg/ml astragalosides for 48 h,the apoptosis rate was higher. CONCLUSIONS:Astragalosides have an anti-tumor effect to some degree by a mechanism which may be related to inhibiting cancer cell proliferation and accelerating apoptosis.

Study of aspirin on proliferation and apoptosis of human lung Adenocarcinoma cell lines SPCA-1 in vivo / 中国药理学通报

AIM To study the effects of ASA on proliferation and apoptosis of human lung Adenocarcinoma cell lines SPCA-1 in vivo. METHODS Cytotoxicity assay was tested by MTT method.Cell cycle was analyzed by flow cytometry(FCM).The morphology of the treated cells was observed by wright exclusion,Hoechest/PI exclusion, electron microscope. Apoptosis landder was evaluated by agarose gel electrophoresis of DNA. RESULTS ASA inhibited SPCA-1 cell proliferation in a time-and dose-dependent fashion(1.0～12.5 mmol?L -1,24 h～72 h). ASA increased the number of cells in G 0/G 1 and G 2/M phases,degrased the population of S phases at on 24 h and incresed apoptosis cells number. CONCLUSION ASA may inhibit the proliferation of SPCA-1 cell lines through effects on cell cycle and apoptosis.