Cao Lijun, Yuan Guixiu, Wang Yaping, Chang Yetian, Xu Junmei, Zou Dingquan, Wei Lai
Department of Anesthesiology, Second Xiangya Hospital, Central South University, Changsha 410011, China.
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2012 Jun;37(6):591-7. doi: 10.3969/j.issn.1672-7347.2012.06.009.
To investigate the liver protection mechanisms of MAPK signaling pathway of limb ischemia preconditioning in the late phase.
Thirty-six adult male New Zealand white rabbits, weighing 1.8-2.0 kg, were randomly divided equally into 3 groups: group C (sham operation), group L (liver ischemia-reperfusion 24 h after limb ischemia preconditioning), group IR (liver ischemia-reperfusion without limb ischemia preconditioning). Serum alanine transaminase (ALT) was measured during ischemia reperfusion. The tissue and cell injury of liver were examined by optical and electron microscopy. Activation of P38MAPK, P44/P42MAPK, and JNK in hepatic tissue was assessed by western blot after 30 min of reperfusion.
Serum ALT and cell injury in the liver as examined by optical and electron microscopy was decreased in group L as compared with the group IR. Phosphorylation of P38MAPK, P44/ P42MAPK, and JNK were all increased significantly after 30 min of reperfusion. Phosphorylation of P38MAPK and JNK was reduced by limb ischemia pre-treatment.
Limb ischemia pre-treatment can induce the late phase of preconditioning in rabbit liver through the inhibition of the phosphorylation of P38MAPK and JNK.
探讨肢体缺血预处理晚期丝裂原活化蛋白激酶（MAPK）信号通路的肝脏保护机制。
将36只体重1.8 - 2.0 kg的成年雄性新西兰白兔随机均分为3组：C组（假手术组）、L组（肢体缺血预处理后24 h行肝脏缺血再灌注）、IR组（未行肢体缺血预处理直接行肝脏缺血再灌注）。在缺血再灌注期间测定血清丙氨酸转氨酶（ALT）水平。通过光学显微镜和电子显微镜检查肝脏组织和细胞损伤情况。再灌注30 min后，采用蛋白质免疫印迹法检测肝组织中P38MAPK、P44/P42MAPK和JNK的激活情况。
与IR组相比，L组血清ALT水平以及光学显微镜和电子显微镜检查的肝脏细胞损伤均有所减轻。再灌注30 min后，P38MAPK、P44/P42MAPK和JNK的磷酸化水平均显著升高。肢体缺血预处理可降低P38MAPK和JNK的磷酸化水平。
肢体缺血预处理可通过抑制P38MAPK和JNK的磷酸化诱导兔肝脏预处理晚期效应。
