Inflammatory mechanisms of Ginkgo Biloba extract in improving memory functions through lncRNA‐COX2/NF‐κB pathway in mice with status epilepticus

PURPOSE: This study was to explore whether Ginkgo biloba extract (GBE) improve memory impairment by alleviating neuroinflammation signaling in mice with status epilepticus. METHODS: The status epilepticus (SE) mice model was established by pilocarpine and treated with 100 mg / kg of GBE for 14 days. Spontaneous alternation of Y‐maze and new object recognition were used to explore memory impairment. To examine glial cell activation, we performed immunohistochemistry and immunofluorescence staining. The activation of NF‐κB signaling and the expression level of lncRNA‐COX2 were detected by Western blot and qRT‐PCR, respectively. Adeno‐associated virus lncRNA‐COX2 was injected into mice for overexpression of lncRNA‐COX2. RESULTS: After GBE treatment, the spontaneous alternation rate and the recognition coefficient in SE mice were both increased. Moreover, activation of glial cells, NF‐κB signaling and lncRNA‐COX2 were significantly decreased in SE mice. In the GBE‐treated SE mice with lncRNA‐COX2 overexpression, NF‐κB signaling was up‐regulated again; the reduced level of inflammation factors was reversed; the GBE‐rescued spontaneous alternation rate of Y‐maze was eliminated. CONCLUSION: Our results suggested that GBE reduces the hippocampal inflammation by down‐regulating lncRNA‐COX2 / NF‐κB signaling in the SE mice, leading to the decrease of neuronal damage and the improvement of memory functions.