Electrophysiologic and anti-inflammatorial effects of cyclooxygenase inhibition in epileptiform activity.

The aim of our study is to investigate the electrophysiological and anti-inflammatory effects of diclofenac potassium on epileptiform activity, which is the liquid form of diclofenac, and frequently used clinically for inflammatory process by inhibiting cyclooxygenase enzyme (COX). Wistar rats aged 2-4 months were divided into Epilepsy, Diazepam, Diclofenac potassium, and Diazepam+diclofenac potassium groups. Diazepam and diclofenac potassium were administered intraperitoneally 30 min after the epileptiform activity was created with penicillin injected intracortically under anesthesia. After the electrophysiological recording was taken in the cortex for 125 min, interleukin-1ß (IL-1ß), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were evaluated by the ELISA in the serums. No change was observed between the groups in serum IL-1ß, IL-6, and TNF-α values. It was observed that the co-administration of diclofenac potassium and diazepam at 51-55, 56-60, 61-65, 111-115, and 116-120 min was more effective in reducing spike amplitude than diclofenac potassium alone (p < 0.05). Single-dose diclofenac potassium did not have an anti-inflammatory effect in epileptiform activity but both diazepam and diclofenac potassium reduced the epileptiform activity.

The Role of the Multi-Inflammatory Index as a Novel Predictor of Hospital Mortality in Acute Ischemic Stroke.

Background and objective Ischemic strokes account for the majority of all strokes. The severity of an acute ischemic stroke (AIS) can be estimated with the help of a number of different scoring systems. However, there is a need for bedside tests that will support the clinical diagnosis and thus help predict the severity of stroke. The research on the multi-inflammatory index (MII), which is calculated using hemogram parameters, has shown immense promise. In light of this, the aim of this study was to establish the association between MII and the severity of AIS. Methods The study included 452 ischemic stroke patients over the age of 18 years who presented to the hospital within 72 hours of the onset of symptoms. Demographic information such as patient age and gender, hemogram parameters, ratios, indices, hospitalization, and mortality status were all recorded. The demographic data, hemogram parameters, neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), and C-reactive protein (CRP)/lymphocyte ratio (CLR), and MII 1, 2, and 3 were compared between surviving and deceased patients. Results The MII-1, MII-2, and MII-3 index values were determined to be significantly low in the patients with Glasgow Coma Scale (GCS) scores of 13-15 compared to those with GCS scores ≤8, and in patients with National Institutes of Health Stroke Scale (NIHSS) score of 1-4 compared to those with scores of 5-14, 15-20, and ≥21. The NLR, CLR, PLR, MII-1, MII-2, and MII-3 index values were significantly higher in the non-survivors (PLR: p=0.004, all other values: p<0.001). The performances of multiple models developed for the mortality cut-off points were evaluated. Together with other factors, Model 1 included the MII-1, Model 2 the MII-2, and Model 3 the MII-3. Although there was no significant difference between the AUC values of the models, the highest sensitivity rate was reached with Model 2 (74.48%), and the highest specificity rate with Model 3 (90.62%). Conclusion Based on our findings, MII is a simple and practical biomarker that can be easily obtained from NLR, PLR, and CRP, and can help in the early detection of poor prognosis in AIS. NLR was found to be superior to PLR and CLR in distinguishing fatal AIS cases.

Oleanolic acid suppresses pentylenetetrazole-induced seizure in vivo.

The aim of this study was to investigate the protective effects of triterpene oleanolic acid on the brain tissue of mice with pentylenetetrazole (PTZ)-induced epileptic seizures. Male Swiss albino mice were randomly separated into five groups as the PTZ, control, and oleanolic acid (10, 30, and 100 mg/kg) groups. PTZ injection was seen to cause significant seizures compared with the control group. Oleanolic acid significantly prolonged the latency to onset of myoclonic jerks and the duration of clonic convulsions, and decreased mean seizure scores following PTZ administration. Pretreatment with oleanolic acid also led to an increase in antioxidant enzyme activity (CAT and AChE) and levels (GSH and SOD) in the brain. The data obtained from this study support oleanolic acid may have anticonvulsant potential in PTZ-induced seizures, prevent oxidative stress and protect against cognitive disturbances. These results may provide useful information for the inclusion of oleanolic acid in epilepsy treatment.