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目的 探讨茶多酚(TP)对心搏骤停(CA)大鼠心肺复苏(CPR)后脑组织c-Jun氨基末端激酶1/2(JNK1/2)磷酸化和凋亡相关因子表达的影响.方法 按随机数字表法将健康雄性SD大鼠分为假手术(Sham)组(n=6)、CA组(n=12)、TP组(n=12).CA组和TP组经食道交流电刺激诱发心室纤颤(室颤), CA 5 min后行CPR,待自主循环恢复(ROSC)后即刻分别静脉注射10 mg/kg生理盐水(CA组)或TP(TP组),于ROSC后12、72h各取6只大鼠脑皮质备检;Sham组不诱导室颤,于72h取脑皮质备检.采用蛋白质免疫印迹试验(Western Blot)检测脑组织磷酸化JNK1/2(p-JNK1/2)、JNK1/2、天冬氨酸特异性半胱氨酸蛋白酶3 (caspase-3)及凋亡基因Bax、Bcl-2的表达;原位末端缺刻标记法(TUNEL)检测细胞凋亡情况;免疫荧光双染检测p-JNK/TUNEL双阳性细胞数.结果 与Sham组比较,CA组脑组织JNK磷酸化水平增高,caspase-3、Bax表达增加,Bcl-2表达降低,ROSC 72h镜下观察凋亡细胞明显增多.与CA组比较,TP组ROSC后12、72h JNK磷酸化水平明显下降(p-JNK1/2与JNK1/2比值:3.200±0.060比5.700±0.210,1.400±0.060比5.400±0.090,均P<0.05),caspase-3、Bax表达明显下调〔caspase-3(灰度值):42.00±5.23比54.00±7.84, 38.74±4.60比58.68±7.19;Bax(灰度值):38.04±6.21比68.76±6.08,58.84±7.99比70.03±7.36,均P<0.05〕, Bcl-2表达明显上调(灰度值:37.36±3.11比28.47±7.46,48.78±6.55比29.54±3.13,均P<0.05),72h细胞凋亡率明显降低〔(31.14±4.51)%比(45.87±3.95)%,P<0.01〕,p-JNK/TUNEL双阳性细胞与TUNEL细胞比值明显降低(10.00±0.85比52.70±3.05,P<0.01).结论 TP抑制CA大鼠CPR后的神经细胞凋亡与其抑制JNK1/2磷酸化有关.“,”Objective To study the effect of tea polyphenols (TP) on c-Jun N-terminal kinase 1/2 (JNK1/2) phosphorylation and cell apoptosis in brain tissues in rats with cardiac arrest (CA) following cardiopulmonary resuscitation (CPR). Methods Healthy male Sprague-Dawley (SD) rats were randomly divided into sham group (n = 6), CA group (n = 12), and TP group (n = 12). The rats in CA and TP groups were induced ventricular fibrillation (VF) via esophagus stimulation with alternating current. Five minutes after CA, CPR was performed. Once restoration of spontaneous circulation (ROSC) was gained, normal saline (NS) and TP were injected intravenously in CA and TP groups with 10 mg/kg, respectively. Cortex of 6 rats in each group was harvested at 12 hours and 72 hours after ROSC. Cortex of sham group was harvested at 72 hours after operation without VF induction. The expressions of phosphorylated JNK1/2 (p-JNK1/2), JNK1/2, caspase-3, Bax and Bcl-2 were measured by Western Blot. Cell apoptosis was detected by TdT-mediated dUTP nick end labeling (TUNEL), and p-JNK/TUNEL double positive cells were detected by fluorescence double staining. Results Compared with sham group, the expressions of p-JNK, caspase-3 and Bax were increased, the expression of Bcl-2 was declined, and the apoptotic cells were significantly increased at 72 hours after ROSC in CA group. Compared with CA group, the phosphorylation of JNK was significantly declined at 12 hours and 72 hours after ROSC in TP group (the ratio of p-JNK1/2 and JNK1/2: 3.200±0.060 vs. 5.700±0.210, 1.400±0.060 vs. 5.400±0.090, both P < 0.05), the expressions of caspase-3 and Bax were decreased [caspase-3 (gray value): 42.00±5.23 vs. 54.00±7.84, 38.74±4.60 vs. 58.68±7.19; Bax (gray value): 38.04±6.21 vs. 68.76±6.08, 58.84±7.99 vs. 70.03±7.36, all P < 0.05], the expression of Bcl-2 was increased (gray value: 37.36±3.11 vs. 28.47±7.46, 48.78±6.55 vs. 29.54±3.13, both P <0.05); the cell apoptosis rate was reduced at 72 hours [(31.14±4.51)% vs. (45.87±3.95)%, P < 0.01], and p-JNK/TUNEL double positive cells/TUNEL cells ratio was significantly decreased (10.00±0.85 vs. 52.70±3.05, P < 0.01).Conclusion The inhibition of neuron apoptosis caused by TP after CPR in rats with CA is related to the inhibition of JNK1/2 phosphorylation.