Downregulation of MicroRNA-34c-5p facilitated neuroinflammation in drug-resistant epilepsy.

The transporter protein ABC subfamily G member 2 (ABCG2) is implicated in epilepsy; however, its specific role remains unclear. In this study, we assessed changes in ABCG2 expression and its role in epilepsy both in vitro and in vivo. We observed an instantaneous increase in ABCG2 expression in epileptic animals and cells. Further, ABCG2 overexpression significantly suppressed the oxidative stress and apoptosis induced by glutamate, kainic acid (KA), and lipopolysaccharide (LPS) in neuronal and microglia cells. Furthermore, inhibiting ABCG2 activity offset this protective effect. ABCG2-deficient mice (ABCG2–/–) showed shorter survival times and decreased survival rates when administered with pentylenetetrazole (PTZ). We also noticed the accumulation of signal transducer and activator of transcription 1 (STAT1) and decreased phosphorylation of mammalian target of rapamycin kinase (mTOR) along with increased ISGylation in ABCG2–/– mice. ABCG2 overexpression directly interacted with STAT1 and mTOR, leading to a decrease in their ISGylation. Our findings indicate the rapid increase in ABCG2 expression acts as a shield in epileptogenesis, indicating ABCG2 may serve as a potential therapeutic target for epilepsy treatment. 

ABCG2 shields against epilepsy, relieves oxidative stress and apoptosis via inhibiting the ISGylation of STAT1 and mTOR

Abstract Sugammadex (SUG) is a modified γ-cyclodextrin molecule used in patients under general anesthesia to reverse the effects of neuromuscular blocking agents. Besides, recent studies have shown that SUG has positive effects on the nervous system. However, its effect on seizures is still unclear. The current study aimed to examine the effects of SUG on pentylenetetrazole (PTZ)-induced epileptic seizures in mice. The mice were randomly divided into 4 groups. Group 1 was control, group 2 was administered saline (1 mL/kg serum physiologic), and Groups 3 and 4 were administered vortioxetine (150 and 300 mg/kg). Pentylenetetrazole (60 mg/kg) was given to induce seizures 30 min after saline or drug administration except for the control group. Total oxidant status (TOS) and total antioxidant status (TAS) levels in the hippocampus and cortex were measured using a commercial kit. 8-hydroxydeoxyguanosine (8-OHdG), 4-hydroxynonenal (4-HNE), 3,3 dityrosine, caspase-3, apoptosis-inducing factor (AIF), and light chain 3 (LC3B) levels in the hippocampal CA1 region after seizures were evaluated immunohistochemical staining. SUG reduced seizure stages and increased epileptic seizure onset times. Moreover, it decreased TOS levels and increased TAS levels in the hippocampus and cortex. Besides, after seizures, it reduced 4-HNE, 3,3 dityrosandine, caspase-3, and LC3B immunohistochemical scores in the hippocampal CA1 region. SUG has protective effects on pentylenetetrazole-induced seizures in mice, with alleviated seizures, oxidative stress, apoptosis, and autophagy. The anticonvulsant mechanism of SUG may be related to the inhibition of the oxidative stress pathway. 

/pdf/the-effects-of-sugammadex-on-pentylenetetrazole-induced-is66jr4w.pdf

The effects of sugammadex on pentylenetetrazole-induced seizures in mice

Unveiling the Protective Potential of Sugammadex against PTZ-Induced Epileptic Seizures in Mice: A Comprehensive Study on Oxidative Stress, Apoptosis, and Autophagy

Resistance to valproic acid (VPA) is a major challenge for epilepsy treatment. We aimed to explore the mechanism underlying this resistance.

https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/cns.14008

Overexpression of Homer1b/c induces valproic acid resistance in epilepsy

Autophagy associated with the efficacy of valproic acid in PTZ-induced epileptic rats

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Autophagy associated with the efficacy of valproic acid in PTZ-induced epileptic rats