ABSTRACT
OBJECTIVE:To study the effects of anisodine hydrobromide on cell apoptosis and extracellular signal-regulated pro-tein kinase 1/2 (ERK1/2) phosphorylation (p-ERK1/2) level in brain tissue of model rats with acute cerebral ischemia-reperfusion injury. METHODS:Rats were randomly divided into sham operation group,model group,positive control group(nimodipine 1.0 mg/kg),anisodine hydrobromide high-dose,medium-dose,low-dose,extreme low-dose groups(1.2,0.6,0.3,0.15 mg/kg),8 in each group. Suture method was used to establish the rat models with acute cerebral ischemia-reperfusion injury. Rats were intrave-nously injected once in tail at 2nd of ischemia and 6th of reperfusion. Then adenosine triphosphate (ATP) enzyme activity,Ca2+content,cell apoptosis in brain tissue,p-ERK1/2 protein expression in brain tissue,and p-ERK1/2/total ERK1/2 (t-ERK1/2) pro-portion in brain tissue of rats were detected after 22 h of reperfusion. RESULTS:Compared with sham operation group,ATP en-zyme activity in brain tissue of rats in model group was obviously decreased,Ca2+ content was obviously increased,density of cell apoptosis in brain tissue was obviously increased,with statistical significances(P<0.01). Compared with model group,density of cell apoptosis in brain tissue was obviously decreased in each administration group;Ca2+ contents in brain tissue of rats in positive control group,anisodine hydrobromide high-dose,low-dose groups were obviously decreased;and p-ERK1/2/t-ERK1/2 proportion in brain tissue of rats in anisodine hydrobromide high-dose,low-dose,extreme low-dose groups were obviously increased,with sta-tistical significances(P<0.05 or P<0.01);the other differences were not statistically significant(P>0.05). CONCLUSIONS:An-isodine hydrobromide can inhibit the cell apoptosis in brain tissue of model rats with acute cerebral ischemia-reperfusion injury,andthe mechanism may be related with activating ERK1/2 signal pathway and regulating ATP enzyme activity to decrease the Ca2+content in the brain tissue.
ABSTRACT
OBJECTIVE:To study the effects of anisodine hydrobromide on cell apoptosis and extracellular signal-regulated pro-tein kinase 1/2 (ERK1/2) phosphorylation (p-ERK1/2) level in brain tissue of model rats with acute cerebral ischemia-reperfusion injury. METHODS:Rats were randomly divided into sham operation group,model group,positive control group(nimodipine 1.0 mg/kg),anisodine hydrobromide high-dose,medium-dose,low-dose,extreme low-dose groups(1.2,0.6,0.3,0.15 mg/kg),8 in each group. Suture method was used to establish the rat models with acute cerebral ischemia-reperfusion injury. Rats were intrave-nously injected once in tail at 2nd of ischemia and 6th of reperfusion. Then adenosine triphosphate (ATP) enzyme activity,Ca2+content,cell apoptosis in brain tissue,p-ERK1/2 protein expression in brain tissue,and p-ERK1/2/total ERK1/2 (t-ERK1/2) pro-portion in brain tissue of rats were detected after 22 h of reperfusion. RESULTS:Compared with sham operation group,ATP en-zyme activity in brain tissue of rats in model group was obviously decreased,Ca2+ content was obviously increased,density of cell apoptosis in brain tissue was obviously increased,with statistical significances(P<0.01). Compared with model group,density of cell apoptosis in brain tissue was obviously decreased in each administration group;Ca2+ contents in brain tissue of rats in positive control group,anisodine hydrobromide high-dose,low-dose groups were obviously decreased;and p-ERK1/2/t-ERK1/2 proportion in brain tissue of rats in anisodine hydrobromide high-dose,low-dose,extreme low-dose groups were obviously increased,with sta-tistical significances(P<0.05 or P<0.01);the other differences were not statistically significant(P>0.05). CONCLUSIONS:An-isodine hydrobromide can inhibit the cell apoptosis in brain tissue of model rats with acute cerebral ischemia-reperfusion injury,andthe mechanism may be related with activating ERK1/2 signal pathway and regulating ATP enzyme activity to decrease the Ca2+content in the brain tissue.