Boychuk T M, Nika O M, Tkachuk S S
Fiziol Zh (1994). 2016;62(6):25-33. doi: 10.15407/fz62.06.025.
The dynamics of the balance of indices of pro- and p53- Bcl-2 anti-apoptotic processes in the hippocampus of rats with experimental diabetes mellitus (DM) complicated by incomplete global cerebral ischemia-reperfusion was investigated. It is shown that p53 proapoptotic processes in animals without diabetes after 20 minutes of ischemia/l hour reperfusion in all fields of the hippocampus are activated in the background of increasing Bcl-2 antiapoptotic processes in the fields CAl, CA2, CA4 and depression of it - in the CA3 field. In the early postischemic period in rats with DM activity of the p53-proapoptotic processes in fields CAl, CA3, CA4 significantly exceeds that in non-diabetic rats (area of p53- IRM increases on 110, 60 and 27 %), and was significantly lower than that detected in CA2 field. On the 12th day of post-ischemic period, activation of apoptosis in field CAl occurs in the background of inert antiapoptotic processes, in animals without diabetes, as well as in diabetic rats, but the indicators characterizing of apoptotic activity in rats with diabetes were higher (specific contents of p53 protein and area ofp53 -IRM increases on 38 and 43 %). During this period, in the CA2 region of the non-diabetic animals, some depression of the antiapoptotic processes with a slight predominance of proapoptotic processes was detected. In the field of CA3 region of rats without diabetes, the retention of activity of proapoptotic processes and the deepening in the dynamics of depression of antiapoptotic processes were showed. In rats with DM, the oppression of both mechanisms with a significant depression of antiapoptotic processes was observed. On the 12th day of experiment in the field CA4, the most balanced relationship were detected between the studied of the processes due to their parallel and unidirectional changes both in the rats without diabetes as well as with DM. The results point on the modifying effect ofDM on susceptibility ofhippocampal fields to ischemic-reperfusion injury.
研究了实验性糖尿病（DM）并发不完全性全脑缺血再灌注大鼠海马中促凋亡和p53 - Bcl - 2抗凋亡过程指标平衡的动态变化。结果表明，在无糖尿病动物中，缺血20分钟/再灌注1小时后，海马各区域p53促凋亡过程被激活，同时CAl、CA2、CA4区Bcl - 2抗凋亡过程增强，而CA3区Bcl - 2抗凋亡过程受到抑制。在DM大鼠缺血后早期，CAl、CA3、CA4区p53促凋亡过程的活性显著高于非糖尿病大鼠（p53 - IRM面积增加110%、60%和27%），且显著低于CA2区。在缺血后第12天，无糖尿病动物和DM大鼠的CAl区均在抗凋亡过程惰性的背景下发生凋亡激活，但DM大鼠的凋亡活性指标更高（p53蛋白的特异性含量和p53 - IRM面积增加38%和43%）。在此期间，非糖尿病动物的CA2区检测到抗凋亡过程略有抑制，促凋亡过程略有占优。在无糖尿病大鼠的CA3区，促凋亡过程活性持续存在，抗凋亡过程抑制加深。在DM大鼠中，两种机制均受到抑制，抗凋亡过程显著降低。在实验第12天，CA4区在无糖尿病和DM大鼠中，由于所研究过程的平行和单向变化，检测到最平衡的关系。结果表明DM对海马区域对缺血再灌注损伤的易感性具有调节作用。
