Stroke is one of the leading causes of death and disability worldwide, and the majority of the cases are ischemic stroke. However, it still lacks effective treatment except for thrombolytic therapy in an extremely narrow time window. Increased evidence suggests that histone deacetylase 4 (HDAC4) was dysregulated in ischemic stroke, which plays a key role in the pathogenesis of ischemic stroke and post-stroke recovery by affecting neuronal death, angiogenesis, and neurogenesis. Therefore, we aim to review the dysregulation of HDAC4 in ischemic stroke and the role of dysregulated HDAC4 in the pathogenesis of ischemic stroke. Furthermore, the therapeutic potential of modulating HDAC4 in ischemic stroke is discussed.

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The aim of this study was to determine the effects of VEGF treatment on focal cerebral ischemia in rats. Rats were administered PBS or VEGF at concentrations of 10, 20 or 30 µg/ml. The effects of VEGF on the rat infarct volume and neurological deficits were investigated. Transmission electron microscopy was used to observe the ultrastructure of the cerebral cortex. Treatments with VEGF reduced the infarct volume and improved neurological functions. VEGF increased microvessel generation and also inhibited apoptosis in the cerebral cortex and basal ganglia. For the rats in the 30 µg/ml VEGF group, an even higher number of proliferative endothelial cells were observed by electron microscopy. In conclusion, VEGF treatment has protective effects on focal cerebral ischemia in rats.

In this study, we investigated the protective effect of l-homocarnosine, l-carnosine, and anserine (HCA) on seizure-induced brain injuries. We evaluated the protective effect of HCA on brain oxidative damage in a pentylenetetrazole (PTZ)-induced epilepsy model using ovariectomized (OVX) rats. The experimental groups were as follows: group I, sham; group II, sham + PTZ; group III, sham + HCA + PTZ; group IV, OVX; group V, OVZ + PTZ; and group VI, OVX + HCA + PTZ. We determined the levels of lipid peroxidation, glutathione peroxidase (Gpx), reduced glutathione (GSH), catalase, superoxide dismutase (SOD), and thiol in brain hippocampal and cortical tissue. The biochemical markers were significantly altered in the brain tissue of OVX rats. HCA supplementation significantly reduced lipid peroxidation and increased GSH, Gpx, SOD, catalase, and thiol levels in PTZ-treated OVX rats. Rats with an ovariectomy showed a significant protective effect against PTZ through elevation of the latency of generalized tonic-clonic seizures (GTCS). HCA substantially increased minimal clonic seizure and GTCS latency in the OVX-PTZ and sham-PTZ groups. In summary, our experimental data indicate that combined supplementation of HCA substantially increased anticonvulsant activity. Moreover, combined HCA supplementation reduced oxidative damage by decreasing lipid peroxidation and increasing antioxidant levels in the brain of a PTZ-induced seizure rodent model.