Abstract:Objective To investigate the protective effect of paeoniflorin on nerve injury in rats with acute cerebral infarction by activating the liver kinase B1 ( LKB1) /5’-amp activated protein kinase (AMPK) signaling pathway. Methods An acute cerebral infarction model was established by occlusion of the middle cerebral artery in rats using sutures, and the rats were randomly divided into a Model group, Paeoniflorin (10 mg/ kg) group, AMPK inhibitor Compound C (CC) (0. 2 mg/ kg) group, and Paeoniflorin (10 mg/ kg) + CC (0. 2 mg/ kg) group, with 12 animals per group. In addition, 12 rats were separated from the common carotid artery and external carotid artery without the suture plug and used as the Sham group. After group administration, a Morris water maze test was used to evaluate the cognitive function of the rats. Triphenyltetrazolium chloride (TTC) staining was used to detect the cerebral infarction of rats in each group. TUNEL staining was used to determine the hippocampal neuron apoptosis rate of rats in each group. Kits were used to measure the levels of serum inflammatory factor inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β) levels, brain catalase (CAT), reactive oxygen species (ROS), and malondialdehyde (MDA) in the brain tissues of the rats. Western blotting was used to detect the expression of apoptosis-related proteins B-cell lymphoma-2 (Bcl-2), BCL2-associated X protein (Bax), and LKB1/ AMPK pathway related proteins (p-LKB1/ LKB1, p-LKB1/ LKB1, p-AMPK/ AMPK) in the brain tissues. Results Compared with the Sham operation group, the number of times crossing the original platform, residence time in the original platform quadrant, brain tissue CAT content, p-LKB1/ LKB1, p-AMPK/ AMPK, and Bcl-2 expression levels in the Model group were significantly less ( P < 0. 05), and the cerebral infarction area, hippocampal neuron apoptosis rate, serum iNOS and IL-1β levels, brain tissue ROS and MDA content, and Bax expression level were significantly greater ( P < 0. 05). Compared with the Model group, the number of times crossing the original platform, residence time in the original platform quadrant, brain tissue CAT content, p-LKB1/ LKB1, p-AMPK/ AMPK, and Bcl-2 expression levels in the Paeoniflorin group were significantly greater ( P < 0. 05), the cerebral infarction area, hippocampal neuron apoptosis rate, serum iNOS and IL-1β levels, brain tissue ROS and MDA contents, and Bax expression level were significantly less ( P < 0. 05). CC can reverse the protective effect of paeoniflorin in a rat cerebral infarction. Conclusions Paeoniflorin may activate the LKB1/ AMPK signal to prevent the occurrence and development of inflammation, reduce the oxidative stress level, reduce brain tissue infarction and hippocampal neuronal apoptosis in rats, improve cognitive function, and play a role in protecting nerves. CC can reduce the protective effect of paeoniflorin in a rat cerebral infarction. 【Keywords】 paeoniflorin; liver kinase B1/5’-amp activated protein kinase; acute cerebral infarction; nerve