CAJ | 학술논문

目的：比较缺血后适应与缺血再灌注（ IR）条件下海马组织内抗凋亡通路JAK2-STAT3-BCL2的表达及激活情况，并比较两种条件下的小鼠海马组织细胞凋亡及认知水平，同时在抑制JAK2、STAT3的条件下观察其对缺血后适应的脑保护作用的影响。方法用水迷宫试验比较两组小鼠认知功能差异；用Western blot方法测定相关蛋白的表达；用TUNEL染色比较细胞凋亡水平；用特异性抑制剂WP1066观察在JAK2、STAT3受抑制的条件下缺血后适应的脑保护效果。结果在缺血后适应的条件下小鼠海马组织中JAK2-STAT3-BCL2通路被明显激活。缺血后适应组JAK2、STAT3、p-JAK2、p-STAT3、BCL2表达均升高（均P＜0．05），海马组织细胞的凋亡程度明显减轻，凋亡细胞数明显较IR组降低（ P＜0．01），凋亡相关蛋白及caspase-3、Bax表达明显降低（均P＜0．05）。认知功能损害程度指标（隐藏平台实验与空间探索实验）水迷宫逃避潜伏期以及进入靶象限占比与IR组相比差异有统计学意义（P＜0．01，P＜0．05）。在抑制JAK2、STAT3的条件下缺血后适应的认知保护作用下降，水迷宫逃避潜伏期以及进入靶象限占比与缺血后适应组相比差异有统计学意义（均P＜0．05），细胞凋亡数增多（P＜0．05），JAK2、STAT3、p-JAK2、p-STAT3、BCL2表达下降，而凋亡相关蛋白caspase-3、Bax 表达上升（均P＜0．05）。结论缺血后适应通过激活JAK2-STAT3-BCL2通路，抑制IR损伤海马组织细胞的凋亡，保护认知功能，继而发挥内源性脑保护作用。
목적：비교결혈후괄응여결혈재관주（ IR）조건하해마조직내항조망통로JAK2-STAT3-BCL2적표체급격활정황，병비교량충조건하적소서해마조직세포조망급인지수평，동시재억제JAK2、STAT3적조건하관찰기대결혈후괄응적뇌보호작용적영향。방법용수미궁시험비교량조소서인지공능차이；용Western blot방법측정상관단백적표체；용TUNEL염색비교세포조망수평；용특이성억제제WP1066관찰재JAK2、STAT3수억제적조건하결혈후괄응적뇌보호효과。결과재결혈후괄응적조건하소서해마조직중JAK2-STAT3-BCL2통로피명현격활。결혈후괄응조JAK2、STAT3、p-JAK2、p-STAT3、BCL2표체균승고（균P＜0．05），해마조직세포적조망정도명현감경，조망세포수명현교IR조강저（ P＜0．01），조망상관단백급caspase-3、Bax표체명현강저（균P＜0．05）。인지공능손해정도지표（은장평태실험여공간탐색실험）수미궁도피잠복기이급진입파상한점비여IR조상비차이유통계학의의（P＜0．01，P＜0．05）。재억제JAK2、STAT3적조건하결혈후괄응적인지보호작용하강，수미궁도피잠복기이급진입파상한점비여결혈후괄응조상비차이유통계학의의（균P＜0．05），세포조망수증다（P＜0．05），JAK2、STAT3、p-JAK2、p-STAT3、BCL2표체하강，이조망상관단백caspase-3、Bax 표체상승（균P＜0．05）。결론결혈후괄응통과격활JAK2-STAT3-BCL2통로，억제IR손상해마조직세포적조망，보호인지공능，계이발휘내원성뇌보호작용。
Objective To comparative ischemic postconditioning and ischemia-reperfusion within the hippocampus of the anti-apoptotic pathway JAK2-STAT3-BCL2 expression and activation , also compare ischemic postconditioning and ischemia-reperfusion(IR) cell apoptosis of hippocampal tissue and cognitive level , while observing its effects on the brain A protective effect in inhibiting JAK2 ,STAT3 conditions .Method Use water maze test cognitive level difference between the two groups of mice; Measured using the Western blot method related protein expression differences;TUNEL staining using comparative level of apoptosis;WP1066 using specific inhibitors observed in JAK2 , STAT3 inhibited .Results Ischemic postconditioning tissue in the hippocampus in the JAK2-STAT3-BCL2 pathway is significantly activated , ischemic postconditioning group JAK 2, STAT3,p-JAK2,p-STAT3,BCL2 expression were increased(all P<0.05),apoptosis of hippocampal tissue cells was significantly reduced , ischemic postconditioning group representing the number of apoptotic cells was significantly reduced compare with IR group ( P<0.01) , and we found that the expression of apoptosis-related protein caspase-3 and Bax was decreased ( all P<0.05);The degree of cognitive impairment indicators ( hidden platform experiments and space exploration experiments ) water maze escape latency and accounting for results into the target quadrant compared with ischemia-reperfusion group was statistically significant (P<0.01, P<0.05);In inhibition JAK2, STAT3 conditions, ischemic postconditioning protective effect of cognitive decline , compared with water maze escape latency and access to adaptation target quadrant for differences were statistically significant(all P<0.05).The levels of apoptotic cells was increased (P<0.05),the expression of JAK2,STAT3,p-JAK2,p-STAT3 and BCL2 were decreased, and expression of the apoptosis-related protein caspase-3 and Bax were increased (all P<0.05).Conclusion Ischemic postconditioning inhibit the apoptosis of hippocampal tissue cells by activating JAK 2-STAT3-BCL2 pathway and protect cognitive function , then play the endogenous protection .