PI3K/Akt信号通路对气腹预处理大鼠肝脏的保护作用

Protective Effect of PI3K / Akt Signaling Pathway on Liver of Pneumoperitoneum Preconditioning Rats

目的:观察气腹预处理后大鼠肝组织中磷脂酰肌醇-3激酶/蛋白激酶B(PI3K/Akt)信号通路的变化。方法:健康SD大鼠30只,随机均分为假气腹组、气腹组和气腹预处理组;气腹组大鼠脐旁插入气腹针并连接SN/REF气腹机充入二氧化碳(CO_2)建立气腹模型(腹压保持在15 mm Hg,持续90 min后解除气腹),气腹预处理组在建立气腹前先进行预处理(充气5 min,放气5 min,重复2次),其余同气腹组;假气腹组大鼠脐旁插入气腹针但不充入CO_2气体;实验结束后处死大鼠;取同一部位肝组织,采用Western Blot检测肝脏中Akt、p-Akt蛋白的表达,采用TUNEL法检测肝细胞凋亡。结果:与假气腹组比较,气腹组大鼠肝脏中Akt及p-Akt的表达显著减少,而肝细胞凋亡率则显著增加,差异具有统计学意义(P<0.01);与气腹组比较,气腹预处理组大鼠肝脏中Akt及p-Akt的表达显著增高,而肝细胞凋亡率则明显较少,差异具有统计学意义(P<0.05)。结论:PI3K/Akt信号通路可能参与了气腹预处理对大鼠肝组织的保护作用。

Objective： To observe the change of PI3K/Akt signaling pathway in liver tissue of pneumoperitoneum preconditioning rats. Methods： 30 healthy SD rats were divided into sham pneumoperitoneum group,pneumoperitoneum group and pneumoperitoneum preconditioning group randomly,10 rats in each group. Inserting the veress beside the navel of rats and connecting SN / REF pneumoperitoneum machine to insufflate CO_2 for 90 minutes to establish the pneumoperitoneum model,abdominal pressure maintained at 15 mm Hg. The pneumoperitoneum preconditioning group was subjected to 5min of insufflation and 5 min of deflation,repeat for 2 times,then following the same practice as pneumoperitoneum group. The rats of sham pneumoperitoneum group were inserted needles but not filling CO_2. Changes of PI3 K / Akt signaling pathway were detected by western blot. The apoptosis of hepatocytes was detected by TUNEL. Results： Comparing with sham pneumoperitoneum group,the expression of total Akt and p-Akt of pneumoperitoneum group were significantly decreased（ P 0. 01）,while the apoptosis of hepatocytes was increased; comparing with pneumoperitoneum group,the expression of total Akt and p-Akt of pneumoperitoneum preconditioning group were significantly increased（ P 0. 05）,while the apoptosis of hepatocytes was decreased. Conclusion： PI3 K / Akt signaling pathway may be involved in the protective effects of pneumoperitoneum preconditioning on liver tissue of rats.