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Cerebral ischemia leads to linguistic and motor dysfunction, as the death of neurons in ischemic core is permanent and non-renewable. An innovative avenue is to induce and/or facilitate reprogramming of adjacent astrocytes into neurons to replace the lost neurons and re-establish brain homeostasis. This study aimed to investigate whether the p-hydroxy benzaldehyde (p-HBA), a phenolic compound isolated from Gastrodia elata Blume, could facilitate the reprogramming of oxygen-glucose deprivation/reperfusion (OGD/R)-damaged astrocytes into neurons. The primary parenchymal astrocytes of rat were exposure to OGD and reperfusion with define culture medium. Cells were then incubated with different concentration of p-HBA (1, 10, 100, 400 μM) and collected at desired time point for reprogramming process analysis. OGD/R could elicit endogenous neurogenic program in primary parenchymal astrocytes of rat under define culture condition, and these so-called reactive astrocytes could be reprogrammed into neurons. However, the neonatal neurons produced by this endogenous procedure could not develop into mature neurons, and the conversion rate was only 1.9%. Treatment of these reactive astrocytes with p-HBA could successfully promote the conversion rate to 6.1%, and the neonatal neurons could develop into mature neurons within 14 days. Further analysis showed that p-HBA down-regulated the Notch signal component genes Dll1, Hes1 and SOX2, while the transcription factor NeuroD1 was up-regulated. The results of this study demonstrated that p-HBA facilitated the astrocyte-to-neuron conversion. This chemical reprogramming was mediated by inhibition of Notch1 signaling pathway and transcriptional activation of NeuroD1. [ABSTRACT FROM AUTHOR]

ABSTRACT Oxidative stress resulting from accumulation of reactive oxygen species (ROS) is involved in cell death associated with neurological disorders such as stroke, Alzheimer's disease and traumatic brain injury. Antioxidant [...]

A variety of conditioning stimuli (e.g. ischemia or hypoxia) can protect against stroke-induced brain injury. While most attention has focused on the effects of conditioning on parenchymal injury, there is considerable evidence that such stimuli also protect the cerebrovasculature, including the blood-brain barrier. This review summarizes the data on the cerebrovascular effects of ischemic/hypoxic pre-, per- and post-conditioning and the mechanisms involved in protection. It also addresses some important questions: Are the cerebrovascular effects of conditioning just secondary to reduced parenchymal injury? How central is endothelial conditioning to overall brain protection? For example, is endothelial conditioning sufficient or necessary for the induction of brain protection against stroke? Is the endothelium crucial as a sensor/transducer of conditioning stimuli?, Competing Interests: Disclosures/conflicts The authors declare they have no conflicts of interest.

The choroid plexuses (CPs) form the blood-cerebrospinal fluid (CSF) barrier (BCSFB) and play an important role in maintaining brain normal function and the brain response to injury. Many neurological disorders are associated with oxidative stress that can impact CP function. This study examined the effects of isothiocyanates, an abundant component in cruciferous vegetables, on H(2)O(2)-induced BCSFB disruption and CP cell death in vitro. It further examined the potential role of a transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2), in isothiocyanate-induced protection. Sulforaphane (SF) significantly reduced H(2)O(2)-induced BCSFB disruption as assessed by transepithelial electrical resistance (29 ± 7% reduction vs. 92 ± 2% decrease in controls) and [(3)H]mannitol permeability. Allyl-isothiocyanate (AITC) had a similar protective effect. H(2)O(2)-induced epithelial cell death was also reduced by these isothiocyanates. In primary CP cells, SF and AITC reduced cell death by 42 ± 3% and 53 ± 10%, respectively. Similar protection was found in a CP cell line Z310. Protection was only found with pretreatment for 12-48 h and not with acute exposure (1 h). The protective effects of SF and AITC were associated with Nrf2 nuclear translocation and upregulated expression of antioxidative systems regulated by Nrf2, including heme oxygenase-1, NAD(P)H quinine oxidoreductase, and cysteine/glutamate exchange transporter. Thus isothiocyanates, as diet or medicine, may be a method for protecting BCSFB in neurological disorders.

Objective: To observe the effect of total flavonoids from Scutellaria amoena on the experimental arrhythmia., Method: Experimental animals anesthetized with 10% chloral hydrate were evenly randomized into control group, positive control group, and low-dose, middle-dose and high-dose total flavonoids groups. The experimental arrhythmia ouabain-induced in guinea pigs and barium chloride or calcium chloride-induced in rats were observed and detected respectively. The result was converted into cumulative dosage of ouabain, in guinea pig model. In rat model, the duration of arrhythmia were detected., Result: hold dosage of ventricular premature heat (VP) and ventricular fibrillation( VF) ouabain-induced in guinea pigs was markedly elevated, and the duration of ventricular tachycardia (VT) barium chloride-induced and VF calcium chloride-induced in rats was postponed by total flavonoids from S. amoena., Conclusion: Total flavonoids from S. amoena has obvious protective effect on drug-induced arrhythmia.