Current research progress of isoflurane in cerebral ischemia/reperfusion injury: a narrative review.

Cerebral ischemia/reperfusion injury is an important factor leading to poor prognosis in ischemic stroke patients. Therefore, it is particularly important to find effective remedial measures to promote the health of patients to return to society. Isoflurane is a safe and reliable anesthetic gas with a long history of clinical application. In recent years, its protection function to human body has been widely recognized, and nowadays isoflurane for cerebral protection has been widely studied, and the stable effect of isoflurane has satisfied many researchers. Basic studies have shown that isoflurane's protection of brain tissue after ischemia/reperfusion involves a variety of signaling pathways and effector molecules. Even though many signaling pathways have been described, more and more studies focus on exploring their mechanisms of action, in order to provide strong evidence for clinical application. This could prompt the introduction of isoflurane therapy to clinical patients as soon as possible. In this paper, several confirmed signaling pathways will be reviewed to find possible strategies for clinical treatment.

P2X4R Contributes to Central Disinhibition Via TNF-α/TNFR1/GABAaR Pathway in Post-stroke Pain Rats.

Central post-stroke pain (CPSP) is a disabling condition in stroke patients. It is a type of neuropathic pain for which the mechanism and relevant drug pathways remain unknown. Inflammatory response and central disinhibition have been suggested recently. Our previous research has shown targeting P2X4 receptors (P2X4R) may be effective in the treatment of CPSP, but the downstream pathway of the P2X4R has not been studied. In this study, we found the increase in tumor necrosis factor alpha (TNF-α) level and endocytosis of surface gamma-aminobutyric acid a receptors (GABAaR) in CPSP, and these effects were inhibited by blocking P2X4R. Furthermore, antagonizing TNF-α can increase surface GABAaR expression and mechanical pain threshold. Meanwhile, knocking down TNFR1 but not TNFR2 reversed the endocytosis of surface GABAaR and alleviated mechanical allodynia. Thus, the neuropathic pain was mediated, in part, through P2X4R/TNF-α/TNFR1/GABAaR signaling, which was induced after stroke. PERSPECTIVE: P2X4R regulates the pathophysiological mechanism of CPSP through central disinhibition mediated by TNF-α/TNFR1. Our results suggest that modulation of P2X4R-TNF-α/TNFR1-GABAaR signaling could provide a new therapeutic strategy to treat CPSP.

Signal-on impedimetric electrochemical DNA sensor using dithiothreitol modified gold nanoparticle tag for highly sensitive DNA detection.

A signal-on impedimetric electrochemical DNA (E-DNA) sensor using gold nanoparticles (AuNPs) as tag was developed for highly sensitive detection of DNA hybridization. A probe ssDNA (PDNA) was immobilized by forming an amide between the -NH2 moiety at the 5'-terminus of PDNA and the -COOH group at self-assembled 11-mercaptoundecanoic acid on a gold electrode. Subsequently, AuNPs were attached to the -SH moiety at the 3'-terminus of the immobilized PDNA by S-Au interaction, and then functionalized with -OH by immersing the electrode in dithiothreitol solution. In the absence of the target DNA, the flexible single-stranded PDNA supports efficient contact between AuNP tag and electrode, ensuring a low electron transfer resistance (Ret) of the E-DNA sensor using the [Fe(CN)6](3-/4-) redox probe. Upon hybridization, a rigid probe-target duplex is formed, which pushes the AuNP tag away from the electrode and increases the distance between AuNP tag and the electrode, thereby increasing the Ret of the E-DNA sensor. Based on hybridization-induced conformational changes, the E-DNA sensor shows an increased Ret response when the target DNA concentration is increased from 5 fM to 500 pM. Furthermore, the E-DNA sensor showed differentiation abilities for single-base mismatch.

A biosensor prepared by co-entrapment of a glucose oxidase and a carbon nanotube within an electrochemically deposited redox polymer multilayer.

A glucose biosensor based on a nanocomposite made by layer-by-layer electrodeposition of the redox polymer into a multilayer containing glucose oxidase (GOx) and single-walled carbon nanotubes (SWCNT) on a screen-printed carbon electrode (SPCE) surface was developed. The objectives of the electrodeposition of redox polymer are to stabilize further the multilayer using a coordinative cross-linked redox polymer and to wire the GOx. The electrochemistry of the layer-by-layer assembly of the GOx/SWCNT/redox polymer nanocomposite was followed by cyclic voltammetry. The resultant biosensor provided stable and reproducible electrocatalytic responses to glucose, and the electrocatalytic current for glucose oxidation was enhanced with an increase in the number of layers. The biosensor displayed a linear range from 0.5 to 6.0mM, a sensitivity of 16.4µA/(mMcm(2)), and a response time of about 5s. It shows no response to 0.05mM of ascorbic acid, 0.32mM of uric acid and 0.20mM of acetaminophen using a Nafion membrane covering the nanocomposite-modified electrode surface.