Long noncoding RNA TUG1 contributes to cerebral ischaemia/reperfusion injury by sponging mir-145 to up-regulate AQP4 expression.

Emerging studies have shown that long noncoding RNA (lncRNA) TUG1 (taurine-up-regulated gene 1) plays critical roles in multiple biological processes. However, the expression and function of lncRNA TUG1 in cerebral ischaemia/reperfusion injury have not been reported yet. In this study, we found that LncRNA TUG1 expression was significantly up-regulated in cultured MA-C cells exposed to OGD/R injury, while similar results were also observed in MCAO model.

Correction to: Inhibition of T cell immunoglobulin and mucin-1 (TIM-1) protects against cerebral ischemia-reperfusion injury.

Following publication of the original article [1], the authors reported that the given name of Liqing Wang was incorrectly published as Liqiang Wang. The original article has been updated.

Inhibition of T cell immunoglobulin and mucin-1 (TIM-1) protects against cerebral ischemia-reperfusion injury.

Background: The T cell Ig domain and mucin domain (TIM)-1 protein expressed on the surface of Th2 cells regulates the immune response by modulating cytokine production. The present study aimed to investigate the role and possible mechanism of TIM-1 in cerebral ischemia-reperfusion injury.

Methods: Western blot was used to detect TIM-1 and apoptosis-related protein expression, whereas TIM-1 mRNA was examined using quantitative real-time reverse transcription PCR.

miR‑29a ameliorates ischemic injury of astrocytes in vitro by targeting the water channel protein aquaporin 4.

Ischemic stroke is the main cause of brain injury and results in a high rate of morbidity, disability and mortality. In the present study, we aimed to determine whether miR‑29a played a protective role in oxygen glucose deprivation (OGD) injury via regulation of the water channel protein aquaporin 4 (AQP4). Real‑time PCR and western blotting were used to assess miR‑29a levels and AQP4 protein levels, respectively.

Upregulation of miR-130b protects against cerebral ischemic injury by targeting water channel protein aquaporin 4 (AQP4).

Altered microRNA regulation has been implicated in the pathogenesis of various disorders, including cerebral ischemia/reperfusion injury (I/RI). However, the regulatory mechanism of miR-130b in cerebral ischemia injury has not been reported. In this study, we explored the role of miR-130b in cerebral ischemia injury and investigated its potential mechanism.

Daphnetin, a natural coumarin derivative, provides the neuroprotection against glutamate-induced toxicity in HT22 cells and ischemic brain injury.

Daphnetin (DAP), a coumarin derivative, has been reported to have multiple pharmacological actions including analgesia, antimalarial, anti-arthritic, and anti-pyretic properties. It is unclear whether DAP has neuroprotective effects on ischemic brain injury. In this study, we found that DAP treatment (i.

A natural coumarin derivative esculetin offers neuroprotection on cerebral ischemia/reperfusion injury in mice.

Previous studies have demonstrated that a natural coumarin compound esculetin (Esc) possesses antioxidant, anti-tumor, and anti-inflammation activities and rescues cultured primary neurons from NMDA toxicity. In this study, we investigated the neuroprotective effects of Esc on cerebral ischemia/reperfusion (I/R) injury in a middle cerebral artery occlusion model in mice. Esc (20 μg) was administered intracerebroventricularly at 30 min before ischemia.

Carvacrol, a food-additive, provides neuroprotection on focal cerebral ischemia/reperfusion injury in mice.

Carvacrol (CAR), a naturally occurring monoterpenic phenol and food additive, has been shown to have antimicrobials, antitumor, and antidepressant-like activities. A previous study demonstrated that CAR has the ability to protect liver against ischemia/reperfusion injury in rats. In this study, we investigated the protective effects of CAR on cerebral ischemia/reperfusion injury in a middle cerebral artery occlusion mouse model.

Antioxidant activity of 7,8-dihydroxyflavone provides neuroprotection against glutamate-induced toxicity.

Glutamate, an excitatory neurotransmitter in the central nervous system, plays an important role in neurological disorders. Previous studies have shown that excess glutamate can cause oxidative stress in a hippocampal HT-22 cell line. 7,8-Dihydroxyflavone (7,8-DHF), a member of the flavonoid family, is a selective tyrosine kinase receptor B (TrkB) agonist that has neurotrophic effects in various neurological diseases such as stroke and Parkinson's disease.