氯化锂对大鼠局灶脑缺血再灌后磷酸化蛋白激酶B(P-Akt)表达的影响

The expression of Phospho-Akt protein in a rat ischemia/reperfusion model and the protective action of postinsult treatment with lithium

Objective to investigate the effects on P-Akt of short-time postinsult treatment with lithium in a rat model of middle cerebral artery occulsion/reperfusion. Methods Inserted with a nylon the right middle cerebral artery of rats was occluded for 1.5h, then recirculation was instituted for various times before death. Experiment 1: SD rats were randomly divided into five subgroups: LI0(0mmol/kg), LI0.5(0.5mmol/kg), LI1(1mmol/kg), LI3(3mmol/kg) andLI5(0mmol/kg), and they were killed two days after ischemic insult. Six rats were used in each subgroup. Experiment 2: SD rats were randomly divided into two groups: ischemia-reperfusion group (IR group) and postinsult treatment with lithium group (LI group, LI = 3mmol/kg). According to the time when they were killed, they were further divided into 4 subgroups: IR6h 、IR1d、IR2d、IR3d;LI6h、LI1d、LI2d、LI3d. Lithium was injected into LI-group’s abdominal cavity one hour after ischemia, and once everyday until they were killed. Saline was injected into IR-group’s with the same treatment. P-Akt protein levels in ischemia hippocampus were detected by Western Blotting. Result ①in Experiment 1, compared to other dosage groups, by 2-day postinsult treatment with lithium, the levels of P-Akt of 3-mmol-per-kg-dosage group were highest; ②in Experiment 2, P-Akt was detectable 6 hours after ischemia in both groups, and the levels of P-Akt expression reached the highest 3 days later. Within the same period, P-Akt was up-regulated more action in LI group than that in IR group. Conclusion our results suggest that postinsult lithium treatment increases the levels of anti-apoptotic protein P-Akt, and it is appropriate with 3mmol/kg.

Objective to investigate the effects on P -Akt of short -time postinsuh treatlnent with lithium in a rat model of middle cerebral artery occulsion/reperfusion. Methods Inserted with a nylon the right middle cerebral artet,y of rats was occluded for 1.5h, then recirculation was instituted for various times before death. Experiment 1： SD rats were randomly divided into five subgroups： LI0（0mmol/kg）, LI0.5（0.5mmol/kg）, LI1（ 1mmol/kg）, LI3（3mmol/kg） and LI5（0mmol/kg）, and they were killed two days after ischemic insult. Six rats were used in each subgroup. Experiment 2： SD rats were randomly divided into two groups： ischemia -reperfusion gronp （IR group） and pestinsult treatment with lithium group （LI group, LI = 3mmol/kg）. According to the time when they were killed, they were further divided into 4 subgroups： IR6h ,IR1d,IR2d,IR3d;LI6h,LI1d,LI2d,LI3d. Lithium was injected into LI -group＇s abdominal cavity one hour ,after ischemia, and once everyday until they were killed. Saline was injected into IR - group＇ s with the same treatment. P - Akt protein levels in is- chemia hippocampus were detected by Western Blotting. Result ①in Experiment 1, compared to other dosage groups, by 2 - day postinsuh treatment with lithium, the levels of P - Akt of 3 -mmol - per - kg - dosage group were highest; ②in Experiment 2, P - Akt was detectable 6 hours after ischemia in both groups, and the levels of P - Akt expression reached the highest 3 days later. Within the same period, P - Akt was up -regulated more action in LI group than that in IR group. Conclusion our results suggest that postinsuh lithium treatment increases the levels of anti -apoptotic protein P- Akt, and it is appropriate with 3mmol/kg.