Sitagliptin might have a myocardial protective effect by inhibiting apoptosis, inflammation, lipid accumulation and myocardial fibrosis in diabetic rats, for a potential role in improving left-ventricular function in diabetes.

Previous studies have demonstrated that baicalein has protective effects against several diseases, which including ischemic stroke. The effect of baicalein on the blood-brain barrier (BBB) in intracerebral hemorrhage (ICH) and its related mechanisms are not well understood. We aimed to investigate the mechanisms by which baicalein may influence the BBB in a rat model of ICH. The rat model of ICH was induced by intravenous injection of collagenase IV into the brain. Animals were randomly divided into three groups: sham operation, vehicle, and baicalein group. Each group was then divided into subgroups, in which the rats were sacrificed at 24 and 72 h after ICH. We assessed brain edema, behavioral changes, BBB leakage, apoptosis, inducible nitric oxide synthase (iNOS), zonula occludens (ZO)-1, Mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB). Treatment with baicalein reduced brain water content, BBB leakage, apoptosis, and neurologic deficits, compared with vehicle. Baicalein also decreased ICH-induced changes in the levels of iNOS but increased the levels of ZO-1. The protective effect of baicalein on the BBB in ICH rats was possibly invoked by attenuated p-38 MAPK and JNK phosphorylation, and decreased activation of the NF-κB signaling pathway, which may have suppressed gene transcription, including iNOS, and eventually decreased formation of peroxynitrite (ONOO). Our results suggest that baicalein exerts a protective effect on BBB disruption in the rat model of ICH. The likely mechanism is via inhibition of MAPKs and NF-κB signaling pathways, leading to decreased formation of iNOS and ONOO, thereby improving neurological function.

Background/Aims: Prior studies demonstrated that pro-inflammatory cytokines (PICs) including IL-1β, IL-6 and TNF-α contribute to regulation of epilepsy-associated pathophysiological processes in the specific brain regions, namely the parietal cortex, hippocampus and amygdala. Moreover, GABA transporter type 1 and 3 (GAT-1 and GAT-3) modulating extracellular GABA levels are engaged in the role played by PICs in epileptogenesis. Note that brain ischemic injury also elevates cerebral PICs. Thus, in this report we examined the effects of nefiracetam (NEF), a pyrrolidone derivative, on the levels of IL-1β, IL-6 and TNF-α, and expression of GAT-1 and GAT-3 in the parietal cortex, hippocampus and amygdala using a rat model of post-ischemic nonconvulsive seizure (NCS). Methods: NCS was evoked by the middle cerebral artery occlusion (MCAO). ELISA and Western Blot analysis were employed to determine the levels of PICs and GAT-1/GAT-3, respectively. Results: MCAO significantly increased IL-1β, IL-6 and TNF-α in the parietal cortex, hippocampus and amygdala as compared with sham control animals (P<0.05 vs. control rats). Also, in these specific brain regions expression of GAT-1 and GAT-3 was amplified; and the levels of GABA were decreased in rats following MCAO (P<0.05 vs. control rats). Systemic administration of NEF significantly attenuated the elevated PICs, amplified GAT-1 and GAT-3 as well as impaired GABA. NEF also attenuated the number of NCS events following MCAO. Conclusion: our data demonstrate that NEF improves post-ischemia evoked-NCS by altering PICs, GABA transporters thereby alleviating GABA in the parietal cortex, hippocampus and amygdala. This support a role for PICs and GABA in engagement of the adaptive responses associated with epileptic activity, but also suggests that NEF has anti-epileptic effects via PICs-GABA mechanisms, having pharmacological implications to target the specific PICs for neuronal dysfunction and vulnerability related to post-ischemic seizures and cognitive impairment.

No abstract

ObjectiveDuring the transition from normal to seizure and then to termination, electroencephalography (EEG) signals have complex changes in time-frequency-spatial characteristics. The quantitative analysis of EEG characteristics and the exploration of their dynamic propagation in this paper would help to provide new biomarkers for distinguishing between pre-ictal and inter-ictal states and to better understand the seizure mechanisms.MethodsThirty-three children with absence epilepsy were investigated with EEG signals. Power spectral and synchronization were combined to provide the time-frequency-spatial characteristics of EEG and analyze the spatial distribution and propagation of EEG in the brain with topographic maps. To understand the mechanism of spatial-temporal evolution, we compared inter-ictal, pre-ictal, and ictal states in EEG power spectral and synchronization network and its rhythms in each frequency band.ResultsPower, frequency, and spatial synchronization are all enhanced during the absence seizures to jointly dominate the epilepsy process. We confirmed that a rapid diffusion at the onset accompanied by the frontal region predominance exists. The EEG power rapidly bursts in 2–4 Hz through the whole brain within a few seconds after the onset. This spatiotemporal evolution is associated with spatial diffusion and brain regions interaction, with a similar pattern, increasing first and then decreasing, in both the diffusion of the EEG power and the connectivity of the brain network during the childhood absence epilepsy (CAE) seizures. Compared with the inter-ictal group, we observed increases in power of delta and theta rhythms in the pre-ictal group (P &lt; 0.05). Meanwhile, the synchronization of delta rhythm decreased while that of alpha rhythm enhanced.ConclusionThe initiation and propagation of CAE seizures are related to the abnormal discharge diffusion and the synchronization network. During the seizures, brain activity is completely changed with the main component delta rhythm. Furthermore, this article demonstrated for the first time that alpha inhibition, which is consistent with the brain’s feedback regulation mechanism, is caused by the enhancement of the network connection. Temporal and spatial evolution of EEG is of great significance for the transmission mechanism, clinical diagnosis and automatic detection of absence epilepsy seizures.