ObjectiveTo compare the curative effect of levetiracetam combined with lamotrigine and sodium valproate on postoperative patients with temporal lobe epilepsy. MethodsA total of 186 postoperative patients with temporal lobe epilepsy during August 2012 to August 2014 in our hospital were divided into levetiracetam combined with lamotrigine group (n=98), and sodium valproate group (n=88) based on postoperative different antiepileptic drugs treatment. Antiepileptic treatment were followed up for 12~48 months.Curative effect and adverse reaction were observed. Reservation rates and incidence rates of adverse reaction were calculated in the two groups. ResultsIn levetiracetam combined with lamotrigine group, EngelⅠratio was 72.4%(71), EngelⅡratio was 17.3%(17), EngelⅢratio was 7.1%(7), and EngelⅣratio was 3.2%(3);in sodium valproate group, EngelⅠratio was 67.0%(59), EngelⅡratio was 21.6%(19), EngelⅢratio was 9.1%(8), and EngelⅣratio was 2.3%(2), and the difference was not statistically significant in the same grade of two groups (P > 0.05).Reservation rate and incidence rate of adverse reaction in levetiracetam combined with lamotrigine group were 90.8%(89) and 15.3%(15) respectively.While those in sodium valproate group were 80.7%(71) and 36.4%(32) respectively.The differences were statistically significant between the two groups (P < 0.05). ConclusionsLevetiracetam combined with lamotrigine treatment on postoperative patients with temporal lobe epilepsy may have better curative effects than sodium valproate treatment, and levetiracetam combined with lamotrigine has its advantage in reservation rate and less adverse reaction.
Objective The study was performed to compare the efficacy and effect on quality of life of sodium valproate (VPA) sustained-release tablets versus topiramate (TPM) in newly diagnosed adult symptomatic epilepsy. Methods This is aprospective, randomized controlled trial on 200 patients newly diagnosed as adult symptomatic epilepsy in Sichuan Province People’s Hospital druing September 2014 to December 2016. The patients were randomly divided into VPA group (n=110) and TPM group (n=90). Then we evaluated the efficacy, retention rate, adverse reactions, and quality of life of the two groups after one year of treatment. Results The total effective rate of VPA group was 69.1%, and the rate of no seizures was 38.2%; the total effective rate of TPM was 62.2%, and the rate of no seizures was 42.2%. No statistically significant difference in the effective rate and no seizure rate was found between the two groups. There was no statistical difference in the retention rate between the two groups(69.1% vs. 65.6%, P>0.05) . The incidence of adverse reactions of VPA was significantly lower than that of TPM (9.1%vs. 20%, P<0.05). The quality of life of the two groups was significantly improved from baseline before treatment. VPA group showed significantly better performance than TPM group on mood and cognitive improvement (P<0.05). Conclusion ① There was no significant difference in efficacy and retention rate between VPA sustained-release tablet and TPM on adult patients with symptomatic epilepsy after one year's treatment; ② The incidence of adverse reactions of TPM group was significantly higher than that of VPA group; ③ VPA sustained-release tablets and TPM can significantly improve the overall quality of life of patients, and VPA sustained-release tablets is significantly better than topiramate on the improvement of emotional and cognitive function.
Objective To investigate the effects of sodium valproate (VPA) in inhibiting Erastin-induced ferroptosis in bone marrow mesenchymal stem cells (BMSCs) and its underlying mechanisms. Methods BMSCs were isolated from bone marrow of 8-week-old Spragur Dawley rats and identified [cell surface antigens CD90, CD44, and CD45 were analyzed by flow cytometry, and osteogenic and adipogenic differentiation abilities were assessed by alizarin red S (ARS) and oil red O staining, respectively]. Cells of passage 3 were used for the Erastin-induced ferroptosis model, with different concentrations of VPA for intervention. The optimal drug concentration was determined using the cell counting kit 8 assay. The experiment was divided into 4 groups: group A, cells were cultured in osteogenic induction medium for 24 hours; group B, cells were cultured in osteogenic induction medium containing optimal concentration Erastin for 24 hours; group C, cells were cultured in osteogenic induction medium containing optimal concentration Erastin and VPA for 24 hours; group D, cells were cultured in osteogenic induction medium containing optimal concentration Erastin and VPA, and 8 μmol/L EX527 for 24 hours. The mitochondrial state of the cells was evaluated, including the levels of malondialdehyde (MDA), glutathione (GSH), and reactive oxygen species (ROS). Osteogenic capacity was assessed by alkaline phosphatase (ALP) activity and ARS staining. Western blot analysis was performed to detect the expressions of osteogenic-related proteins [Runt-related transcription factor 2 (RUNX2) and osteopontin (OPN)], ferroptosis-related proteins [glutathione peroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1), and solute carrier family 7 member 11 (SLC7A11)], and pathway-related proteins [adenosine monophosphate-activated protein kinase (AMPK) and Sirtuin 1 (SIRT1)]. Results The cultured cells were identified as BMSCs. VPA inhibited Erastin-induced ferroptosis and the decline of osteogenic ability in BMSCs, acting through the activation of the AMPK/SIRT1 pathway. VPA significantly reduced the levels of ROS and MDA in Erastin-treated BMSCs and significantly increased GSH levels. Additionally, the expression levels of ferroptosis-related proteins (GPX4, FTH1, and SLC7A11) significantly decreased. VPA also upregulated the expressions of osteogenic-related proteins (RUNX2 and OPN), enhanced mineralization and osteogenic differentiation, and increased the expressions of pathway-related proteins (AMPK and SIRT1). These effects could be reversed by the SIRT1 inhibitor EX527. ConclusionVPA inhibits ferroptosis in BMSCs through the AMPK/SIRT1 axis and promotes osteogenesis.