Objective: To investigate the protective effect and related mechanism of glycyrrhizic acid on hippocampal neuron damage in epileptic rats.
Methods: The rat epilepsy model was made by igniting lithium chloride-pilucapine. After successful modeling, the rats were randomly divided into the epilepsy group and the glycyrrhizic acid group. In addition, the rats without any treatment were used as the normal control group. 12. The damage and apoptosis of rat hippocampal neurons were detected by Nissl method and TUNEL method; the mitochondrial membrane potential of rat hippocampal neurons was detected by JC-1 method; caspase 3 and caspase were detected by colorimetric method 9 activity; Western blot method was used to detect cleaved-caspase 3, 9, B-lymphoma-2 (Bcl-2), Bcl-2-related X protein (Bax), cytochrome C (CytC), apoptosis in rat hippocampus tissue expression of apoptotic protease activator (Apaf-1).
Results: Compared with the normal control group, the number of neurons in the epilepsy group decreased (P < 0.01), the number of TUNEL positive cells increased (P < 0.01), the mitochondrial membrane potential decreased (P < 0.01), the caspase The activities of 3 and 9 were increased (P < 0.01), the expressions of CytC in Bcl-2 and mitochondria were down-regulated (P < 0.01), and the expressions of CytC and Apaf-1 in Bax and cytoplasm were up-regulated (P < 0.01). . Compared with the epilepsy group, the number of neurons in the glycyrrhizic acid group increased (P < 0.01), the number of TUNEL positive cells decreased (P < 0.01), and the mitochondrial membrane potential increased (P < 0.01), and caspase 3, 9 The activity decreased (P < 0.01), the expression of CytC in Bcl-2 and mitochondria was up-regulated (P < 0.01), and the expression of CytC and Apaf-1 in Bax and cytoplasm was down-regulated (P < 0.01).
Conclusion: By blocking the mitochondrial pathway, glycyrrhizic acid can inhibit the damage of hippocampal neurons in epileptic rats.