&lt;p&gt;Hyperbaric oxygen therapy attenuates neuronal apoptosis induced by traumatic brain injury via Akt/GSK3&amp;beta;/&amp;beta;-catenin pathway&lt;/p&gt;

Zhang

et al. 2020

FEBS Open Bio

Postoperative cognitive dysfunction is a common complication in elderly patients after surgeries involving anesthesia, but the underlying mechanisms are poorly understood. Lithium is a conventional treatment for bipolar disorder, which exerts a neuroprotective role in various diseases by inhibiting glycogen synthase kinase‐3β (GSK‐3β) in the brain and spinal cord. However, it is not known whether lithium chloride (LiCl) can protect against cognitive dysfunction induced by sevoflurane (SEV) anesthesia. Here, we examined the effects of LiCl on SEV‐induced cognitive dysfunction in rats and on SEV‐induced neuron apoptosis. We report that anesthesia with SEV significantly impaired memory performance, induced oxidative stress and hippocampal neuron apoptosis, and stimulated GSK‐3β activity. Treatment with LiCl ameliorated SEV‐induced cognitive disorder in rats by inhibiting the GSK‐3β/β‐catenin signaling pathway. In addition, LiCl reduced hippocampal neuron apoptosis and oxidative stress induced by SEV anesthesia. These results suggest that LiCl may have potential for development into a therapeutic agent for treatment of SEV anesthesia‐induced cognitive dysfunction.

Section: Discussionsupporting

confidence: 91%

Lithium chloride ameliorates cognition dysfunction induced by sevoflurane anesthesia in rats

Zhang

et al. 2020

FEBS Open Bio

“…Many studies have explored the potential effects of several medical gases on nerve regeneration, oxidative stress and apoptosis after TBI. Hyperbaric oxygen promotes nerve regeneration and attenuates apoptosis in animal models of TBI and patients . Hydrogen sulphide offered neuroprotection after TBI in mice, together with reduced apoptosis and oxidative stress .…”

Section: Discussionmentioning

confidence: 99%

Hydrogen exerts neuroprotection by activation of the miR‐21/PI3K/AKT/GSK‐3β pathway in an in vitro model of traumatic brain injury

Yin

J Cellular Molecular Medi

et al. 2020

Few studies have explored the effect of hydrogen on neuronal apoptosis or impaired nerve regeneration after traumatic brain injury, and the mechanisms involved in these processes are unclear. In this study, we explored neuroprotection of hydrogen‐rich medium through activation of the miR‐21/PI3K/AKT/GSK‐3β pathway in an in vitro model of traumatic brain injury. Such model adopted PC12 cells with manual scratching. Then, injured cells were cultured in hydrogen‐rich medium for 48 hours. Expression of miR‐21, p‐PI3K, p‐Akt, p‐GSK‐3β, Bax and Bcl‐2 was measured using RT‐qPCR, Western blot analysis and immunofluorescence staining. Rate of apoptosis was determined using TUNEL staining. Neuronal regeneration was assessed using immunofluorescence staining. The results showed that hydrogen‐rich medium improved neurite regeneration and inhibited apoptosis in the injured cells. Scratch injury was accompanied by up‐regulation of miR‐21, p‐PI3K, p‐Akt and p‐GSK‐3β. A miR‐21 antagomir inhibited the expression of these four molecules, while a PI3K blocker only affected the three proteins and not miR‐21. Both the miR‐21 antagomir and PI3K blocker reversed the protective effect of hydrogen. In conclusion, hydrogen exerted a neuroprotective effect against neuronal apoptosis and impaired nerve regeneration through activation of miR‐21/PI3K/AKT/GSK‐3β signalling in this in vitro model of traumatic brain injury.

“…Mice in which TBI was induced were placed in a hyperbaric chamber for 90 min. This regimen reduced the number of apoptotic neurons, as well as the mRNA expression of caspase-3 and the level of cleaved-caspase-3 ( He et al, 2019 ). These effects were associated to an increased expression of β-catenin and decreased expression of GSK3β ( He et al, 2019 ).…”

Section: The Wnt Pathway In Tbimentioning

confidence: 99%

Wnt Pathway: An Emerging Player in Vascular and Traumatic Mediated Brain Injuries

2020

The Wnt pathway, which comprises the canonical and non-canonical pathways, is an evolutionarily conserved mechanism that regulates crucial biological aspects throughout the development and adulthood. Emergence and patterning of the nervous and vascular systems are intimately coordinated, a process in which Wnt pathway plays particularly important roles. In the brain, Wnt ligands activate a cellspecific surface receptor complex to induce intracellular signaling cascades regulating neurogenesis, synaptogenesis, neuronal plasticity, synaptic plasticity, angiogenesis, vascular stabilization, and inflammation. The Wnt pathway is tightly regulated in the adult brain to maintain neurovascular functions. Historically, research in neuroscience has emphasized essentially on investigating the pathway in neurodegenerative disorders. Nonetheless, emerging findings have demonstrated that the pathway is deregulated in vascular-and traumatic-mediated brain injuries. These findings are suggesting that the pathway constitutes a promising target for the development of novel therapeutic protective and restorative interventions. Yet, targeting a complex multifunctional signal transduction pathway remains a major challenge. The review aims to summarize the current knowledge regarding the implication of Wnt pathway in the pathobiology of ischemic and hemorrhagic stroke, as well as traumatic brain injury (TBI). Furthermore, the review will present the strategies used so far to manipulate the pathway for therapeutic purposes as to highlight potential future directions.