JNK信号通路在异氟醚预处理和七氟醚预处理减轻大鼠海马脑片缺氧无糖损伤中的作用

目的 评价c-Jun氨基末端激酶(JNK)信号通路在异氟醚预处理和七氟醚预处理减轻大鼠海马脑片缺氧无糖(OGD)损伤中的作用.方法雄性成年SD大鼠,体重270～290 g,断头处死,剥离海马,制备海马脑片.取大鼠海马脑片96张,采用随机数字表法,将其随机分为8组(n=12):对照组(C组)、OGD组、异氟醚预处理组(Iso组)、七氟醚预处理组(Sevo组)、SP600125+异氟醚预处理组(SP+Iso组)、SP600125+七氟醚预处理组(SP+Sevo组)、二甲基亚砜(DMSO)+异氟醚预处理组(DMSO+Iso组)和DMSO+七氟醚预处理组(DMSO+Sevo组).采用电生理技术,细胞外记录CA1区群锋电位(PS)波幅,计算PS恢复程度.采用碘化丙啶染色法,测定细胞活力.结果 与C组比较,其余各组PS恢复程度和细胞活力降低(P＜0.01);与OGD组比较,Iso组、Sevo组、SP+Iso.组、SP+Sevo组、DMSO+Iso组和DMSO+Sevo组PS恢复程度和细胞活力升高(P＜0.01);与180组比较,SP+Iso组PS恢复程度和细胞活力升高(P＜0.01),DMSO+Iso组PS恢复程度和细胞活力差异无统计学意义(P＞0.05);与Sevo组比较,SP+Sevo组PS恢复程度和细胞活力升高(P＜0.01),DMSO+Sevo组PS恢复程度和细胞活力差异无统计学意义(P＞0.05).结论 异氟醚预处理和七氟醚预处理可通过抑制JNK信号通路,减轻大鼠海马脑片缺氧无糖损伤.

Abstract：

Objective To evaluate the role of c-Jun N-terminal kinase (JNK) signaling pathway in the protective effect of isoflurane preconditioning and sevoflurane preconditioning against oxygen-glucose deprivation (OGD) injury in rat hippocampal slices. Methods Male adult SD rats weighing 270-290 g were anesthetized with ether and decapitated. The hippocampi were removed and sagittally sliced (400 μm thick) and placed in artificial cerebral spinal fluid aerated with 95% O2-5% CO2 . Ninety-six hippocampal slices were randomly divided into 8 groups (n = 12 each): control group (group C), OGD group, isoflurane preconditioning group (group Iso),sevoflurane preconditioning group (group Sevo) , SP600125 + isoflurane preconditioning group (group SP + Iso),SP600125 +sevoflurane preconditioning group (group SP + Sevo), DMSO + isoflurane preconditioning group (group DMSO + Iso) and DMSO + sevoflurane preconditioning group (group DMSO + Sevo). Electrophysiological technique was used to record the amplitude of population spike ( PS) in the stratum pyramidale of CA1 region and the degree of recovery of PS was calculated. The cell viability was determined by propidium iodide staining. Results Compared with group C, the degree of recovery of PS and cell viability were significantly decreased in the other groups ( P ＜ 0.01) . Compared with group OGD, the degree of recovery of PS and cell viability were significantly increased in groups Iso, Sevo, SP+Iso, SP+Sevo, DMSO+ Iso and DMSO + Sevo (P＜ 0.01). Compared with group Iso, the degree of recovery of PS and cell viability were significantly increased in group SP+Iso ( P ＜ 0.01) , while no significant change was found in group DMSO + Iso ( P ＞ 0.05) . Compared with group Sevo, the degree of recovery of PS and cell viability were significantly increased in group SP + Sevo ( P ＜ 0.01) , while no significant change was found in group DMSO + Sevo ( P ＞ 0.05). Conclusion Isoflurane preconditioning and sevoflurane preconditioning can attenuate the OGD injury to rat hippocampal slices through inhibiting JNK signaling pathway.

Role of c-Jun N-terminal kinase signaling pathway in the protective effect of isoflurane preconditioning and sevoflurane preconditioning against oxygen-glucose deprivation injury in rat hippocampal slices

Objective To evaluate the role of c-Jun N-terminal kinase (JNK) signaling pathway in the protective effect of isoflurane preconditioning and sevoflurane preconditioning against oxygen-glucose deprivation (OGD) injury in rat hippocampal slices. Methods Male adult SD rats weighing 270-290 g were anesthetized with ether and decapitated. The hippocampi were removed and sagittally sliced (400 μm thick) and placed in artificial cerebral spinal fluid aerated with 95% O2-5% CO2 . Ninety-six hippocampal slices were randomly divided into 8 groups (n = 12 each): control group (group C), OGD group, isoflurane preconditioning group (group Iso),sevoflurane preconditioning group (group Sevo) , SP600125 + isoflurane preconditioning group (group SP + Iso),SP600125 +sevoflurane preconditioning group (group SP + Sevo), DMSO + isoflurane preconditioning group (group DMSO + Iso) and DMSO + sevoflurane preconditioning group (group DMSO + Sevo). Electrophysiological technique was used to record the amplitude of population spike ( PS) in the stratum pyramidale of CA1 region and the degree of recovery of PS was calculated. The cell viability was determined by propidium iodide staining. Results Compared with group C, the degree of recovery of PS and cell viability were significantly decreased in the other groups ( P ＜ 0.01) . Compared with group OGD, the degree of recovery of PS and cell viability were significantly increased in groups Iso, Sevo, SP+Iso, SP+Sevo, DMSO+ Iso and DMSO + Sevo (P＜ 0.01). Compared with group Iso, the degree of recovery of PS and cell viability were significantly increased in group SP+Iso ( P ＜ 0.01) , while no significant change was found in group DMSO + Iso ( P ＞ 0.05) . Compared with group Sevo, the degree of recovery of PS and cell viability were significantly increased in group SP + Sevo ( P ＜ 0.01) , while no significant change was found in group DMSO + Sevo ( P ＞ 0.05). Conclusion Isoflurane preconditioning and sevoflurane preconditioning can attenuate the OGD injury to rat hippocampal slices through inhibiting JNK signaling pathway.