MEF2D Participates in Microglia-Mediated Neuroprotection in Cerebral Ischemia-Reperfusion Rats.

Objective: Microglial activation is a vital process in the neuroinflammatory response induced by I/R injury. It has been reported that myocyte enhancer factor (MEF)2D expression in activated microglia is associated with microglia-induced inflammatory responses and plays an important role in neuronal survival. This research aimed to investigate the role and mechanism of MEF2D in microglial activation and neuroinflammation in cerebral I/R in vitro and in vivo.

miR-217-regulated MEF2D-HDAC5/ND6 signaling pathway participates in the oxidative stress and inflammatory response after cerebral ischemia.

Multiple factors are known to contribute to the pathogenesis of cerebral ischemic injury, including microRNAs (miRNAs). However, the precise mechanism of miRNAs involvement in cerebral ischemia remains largely unclear. In the current study, we found that miR-217 was significantly upregulated in ischemic stroke models, and the upregulation of miR-217 was associated with the development of post-stroke cognitive impairment.

Effects of niflumic acid on γ-aminobutyric acid-induced currents in isolated dorsal root ganglion neurons of neuropathic pain rats.

Niflumic acid (NFA) is a type of non-steroidal anti-inflammatory drug. Neuropathic pain is caused by a decrease in presynaptic inhibition mediated by γ-aminobutyric acid (GABA). In the present study, a whole-cell patch-clamp technique and intracellular recording were used to assess the effect of NFA on GABA-induced inward current in dorsal root ganglion (DRG) neurons of a chronic constriction injury (CCI) model.