Ursolic Acid Protects Neurons in Temporal Lobe Epilepsy and Cognitive Impairment by Repressing Inflammation and Oxidation

• DOI: 10.3389/fphar.2022.877898
• Publication Date: 2022-05-16T04:52:13Z
• Authors: Kun-mei Liu; Yue Huang; Pan-pan Wan; Yun-hua Lu; Ning Zhou; Juan-juan Li; Chun-yang Yu; Jin-jiang Chou; Lianxiang Zhang; Chun Zhang; Yuan-yuan Qiang; Rui Zhang; Le Guo
• Keywords: Pharmacology; 03 medical and health sciences; antioxidant; 0302 clinical medicine; neuroprotective; Therapeutics. Pharmacology; RM1-950; temporal lobe epilepsy; ursolic acid; cognitive impairment; anti-inflammatory

Temporal lobe epilepsy (TLE) is characterized as an impaired ability of learning and memory with periodic unpredictable seizures. Status epilepticus (SE) one the main causes TLE. Neuroinflammation oxidative stress are directly involved in epileptogenesis neurodegeneration, promoting chronic cognitive deficit. Previous studies have shown that ursolic acid (UA) represses inflammation stress, contributing to neuroprotection. Herein, we demonstrated UA treatment alleviated seizure behavior impairment induced by epilepsy. Moreover, rescued hippocampal neuronal damage, aberrant neurogenesis, ectopic migration, which commonly accompanied occurrence. Our study also remarkably suppressed SE-induced neuroinflammation, evidenced activated microglial cells decreased factors, including TNF-α IL-1β. Likewise, expression levels damage markers phosphorylation (OXPHOS) enzyme complexes mitochondria were downregulated following treatment, suggesting caused high defect mitochondrial function SE. Furthermore, attenuated GABAergic interneuron loss. In summary, our clarified notable anti-seizure neuroprotective properties pilocarpine-induced epileptic rats, mainly achieved abilities anti-inflammation anti-oxidation. indicates potential advantage application ameliorating sequelae.