Yongge Li1, Xiaoming Wei1, Qingchun Liu1, Shifeng Zhang1, Yongchao Deng2, *
1Department Basic Medical, Nan Yang Medical College, Nanyang 473000, Henan Province, China - 2Department of Neurology, the Second Hospital of Jingzhou City, Jingzhou 434000, Hubei Province, China
Objective: To analyse the effect of glycyrrhizin (GL) on kainic acid (KA)-induced hippocampal pathological damage through the HMGB1/TLR4/P-NF-κB pathway.
Methods: Sixty male 21-day-old Sprague Dawley (SD) rats were randomly divided into a control group, a KA group, and a GL group. The control group was injected intraperitoneally with normal saline, the KA group was injected with KA, and the GL group was injected intraperitoneally with KA. The SE and death of mice were observed after modelling, and the time when rats reached grade III attack (SOT) was recorded. After seven days of modelling, the mice were killed, the pathological changes were observed by HE staining, and the expression of the neuronal antinuclear antibody (Neu-N) was detected. RT-PCR was used to detect the expression of HMGB1 and TLR-4 mRNA, and Western blot was used to detect the protein expression of HMGB1, TLR4, and P-NF-κB.
Results: The incidence of SE and mortality in the GL group were 50.00% and 10.00%, respectively, significantly lower than 80.00% and 40.00% of the KA group. Furthermore, the level of SOT in the GL group was significantly higher than in the KA group (P<0.05). The results of HE staining showed that the inclusion bodies of nerve cells in the KA group were shrunk and crimson, the nucleus pyknosis was noticeable, the intercellular space was enlarged, the structure was disordered, some nerve cells were lysed, and the nucleus was dissolved. Nerve degeneration and necrosis were also found in the GL group but with less severity than in the KA group. The number of Neu-N positive cells in the control and GL groups were significantly higher than in the KA group (P<0.05). The HMGB1 and TLR-4 mRNA expression levels were significantly higher in the KA group than in the control and GL groups (P<0.05). The expression levels of TLR-4 and P-NF-κB protein in the KA group were significantly higher than those in the control and GL groups (P<0.05).
Conclusion: GL can slow down KA-induced epilepsy in young rats, inhibit the pathological damage of the hippocampus, and decrease Neu-N positive cells. The mechanism may be related to GL’s regulation of the HMGB1/TLR4/P-NF-κB pathway.
Glycyrrhizin, HMGB1/TLR4/P-NF-κB pathway, immature rats, epilepsy, hippocampus, pathological damage.