lithium-chloride and thymoquinone

Status epilepticus (SE), is characterized by high mortality and morbidity, which can cause neuronal injury, neuronal death and alteration of neuronal networks, Recently, inflammation was shown to play a significant role in SE pathogenesis. And miRNA-146a has been shown to be involved in inflammation and to inhibit inflammatory cytokines through NF-κB pathway. In our study, we investigated the relationship between inflammation and miR-146a expression.. The SE rat model was induced by lithium-pilocarpine. Hematoxylin and eosin staining (H&E) was performed to observe the histopathology of the rat hippocampus. The expression of COX-2, TNF-α, IL-6 and IL-1β were respectively measured by Western blot and Bio-Plex ProTM Assays. The miR-146a expression in hippocampus tissue was measured by Quantitative real-time PCR.. microRNA-146a was highly expressed in the hippocampus of SE rats coupled with increased level of inflammatory cytokines than the normal group. And TQ can attune the expression of inflammatory cytokines, meanwhile, miR-146a was lower in TQ group. The expression of miRNA-146a were positively correlated with the level of inflammatory reaction.. TQ may alleviate the inflammatory reaction by inhibiting the NF-κB signaling pathway. Our study shows that miRNA-146a was involved in the inflammatory response and indicated inflammation severity in SE rats. Therefore, miRNA-146a may serve as a potential biomarker or a therapeutic target in SE.

Topics: Animals; Anticonvulsants; Benzoquinones; Cytokines; Disease Models, Animal; Gene Expression Regulation; Hippocampus; Inflammation; Lithium Chloride; Male; MicroRNAs; Muscarinic Agonists; NF-kappa B; Pilocarpine; Rats; Rats, Sprague-Dawley; Status Epilepticus

Inflammation plays a pivotal role in status epilepticus (SE). Thymoquinone (TQ) is a bioactive monomer extracted from black seed (Nigella sativa) oil, which has anti-inflammatory properties in the context of various diseases. This study explored the protective effects of TQ in SE and used a lithium-pilocarpine model of SE to investigate the underlying mechanism, which was related to inflammation mediated by the NF-κB signaling pathway. In the present study, latency to SE increased in the TQ-pretreated group compared with the SE group, and the incidence of SE was significantly reduced. The seizure severity score measured on the Racine scale was significantly decreased in the TQ group compared with the SE group. Moreover, the results of the behavioral tests suggested that TQ may also have a protective effect on learning and memory functions. Finally, we further investigated the protective mechanism of TQ. The results showed that TQ-pretreatment significantly downregulated the protein levels of COX-2 and TNF-α in the brain, in a manner mediated by the NF-κB signaling pathway. These findings demonstrate that TQ attenuates convulsant activity via an anti- inflammation signaling pathway in a model of SE.

Topics: Animals; Anti-Inflammatory Agents; Benzoquinones; Cerebral Cortex; Cytokines; Electroencephalography; Hippocampus; Lithium Chloride; Male; Maze Learning; Memory; NF-kappa B; Pilocarpine; Rats, Sprague-Dawley; Seizures; Signal Transduction; Status Epilepticus