[Animal modeling] - protective effect of paeoniflorin on nerve injury in rats with acute cerebral infarction by activating LKB1/AMPK signal pathway

  Objective To investigate the protective effect of paeoniflorin on nerve injury in rats with acute cerebral infarction by activating hepatic kinase B1 (LKB1)/5 '- adenosine phosphate activated protein kinase (AMPK) signal pathway.

  Methods Rat models of acute cerebral infarction were established by occlusion of middle cerebral artery with thread embolism. They were randomly divided into model group, paeoniflorin (10 mg/kg) group and AMPK inhibitor CC (0 2 mg/kg) group, paeoniflorin (10 mg/kg)+CC (0 2 mg/kg) group, 12 rats in each group, and 12 rats in the other group were separated from the common carotid artery and external carotid artery, and were set as sham operation group without plug. After treatment in groups, the cognitive function of rats was evaluated by Morris water maze test; The cerebral infarction of rats in each group was detected by triphenyl tetrazolium chloride (TTC) staining; The apoptosis rate of hippocampal neurons in each group was measured by TUNEL staining; The serum inflammatory factor-inducible nitric oxide synthase (iNOS) and interleukin-1 in rats of each group were measured with the kit β ( IL-1 β) Levels of catalase (CAT), reactive oxygen species (ROS) and malondialdehyde (MDA) in brain tissue; The expression of apoptosis-related protein B lymphoblastoma-2 (Bcl-2), BCL2-related X protein (Bax) and LKB1/AMPK pathway related protein (p-LKB1/LKB1, p-AMPK/AMPK) in brain tissue of rats in each group were detected by Western blot.

  Results Compared with the sham-operated group, the number of times the rats crossed the original platform, the residence time in the original platform quadrant, the CAT content in brain tissue, the expression level of p-LKB1/LKB1, p-AMPK/AMPK, and Bcl-2 in the model group were significantly decreased (P<0. 05) 05), cerebral infarction area, hippocampal neuron apoptosis rate, serum iNOS and IL-1 β The levels of ROS, MDA and Bax expression in brain tissue were significantly increased (P<0. 05) 05)。 Compared with the model group, the number of times paeoniflorin group rats crossed the original platform, the residence time in the original platform quadrant, the CAT content in brain tissue, and the expression levels of p-LKB1/LKB1, p-AMPK/AMPK, and Bcl-2 were significantly higher (P<0. 05) 05), cerebral infarction area, hippocampal neuron apoptosis rate, serum iNOS and IL-1 β The levels of ROS, MDA and Bax expression in brain tissue decreased significantly (P<0 05)。 CC can reduce the protective effect of paeoniflorin on cerebral infarction in rats.

  Conclusion Paeoniflorin may inhibit the occurrence and development of inflammation, reduce the level of oxidative stress, alleviate the cerebral infarction and hippocampal neuron apoptosis in rats, improve their cognitive function, and play a role in protecting the nerves by activating the LKB1/AMPK signal pathway. CC can reduce the protective effect of paeoniflorin on cerebral infarction in rats.