Normobaric Hyperoxia Preconditioning Induces Changes in the Brain Lipidome

Faezi, Masoumeh; Bigdeli, Mohammad Reza; Mirzajani, Fateme; Ghasempour, Alireza

doi:10.2174/1567202612666150819100746

Cited by 4 publications

(3 citation statements)

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“…It is well-established that Cer is involved in oxidative stress, inflammation, and/or cell death, which contribute to the development of AD. Apoptosis is stimulated by Cer though the inhibition of mitochondrial electron transport and cytochrome release (Faezi et al, 2015). High levels of Cer in the brain can promote inflammatory pathways and exert negative effects on neurons during the aging process (Cutler et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Metabolomic and Lipidomic Profiling of Preoperative CSF in Elderly Hip Fracture Patients With Postoperative Delirium

Han

Zhang

Liu

et al. 2020

Front. Aging Neurosci.

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Objective: To investigate dysregulated molecules in preoperative cerebrospinal fluid (CSF) of elderly hip fracture patients with postoperative delirium (POD), in order to identify potential pathological mechanisms and biomarkers for pre-stage POD. Materials and Methods: This nested case control study used untargeted metabolomic and lipidomic analysis to profile the preoperative CSF of patients (n = 40) who developed POD undergone hip fracture surgery (n = 10) and those who did not (n = 30). Thirty Non-POD patients were matched to 10 POD patients by age (± 2 years) and Mini Mental State Examination score (± 2 points). CSF was collected after successful spinal anesthesia and banked for subsequent analysis. On the first two postoperative days, patients were assessed twice daily using the Confusion Assessment Method-Chinese Revision. CSF samples from the two groups were analyzed to investigate possible relevant pathological mechanisms and identify candidate biomarkers. Results: Demographic characteristics of the groups were matched. Eighteen metabolites and thirty-three lipids were dysregulated in the preoperative CSF of POD patients. Pathway enrichment analysis revealed perturbations in D-glutamine and D-glutamate metabolism; glycerophospholipid metabolism; alanine, aspartate and glutamate metabolism; sphingolipid metabolism; histidine metabolism; and arginine biosynthesis at the pre-delirium stage. Receiver operating characteristic curve analysis indicated that phosphatidylethanolamine (PE, 40:7e), with an area under the curve value of 0.92, is a potential biomarker for POD. Conclusion: Multiple pathological mechanisms in the POD group were involved before surgery, including neuroinflammation, oxidative stress, and energy metabolism disorders induced by hypoxia, as well as neurotransmitter imbalances such as increased dopamine and glutamate, and decreased glutamine. These metabolic abnormalities potentially increase the fragility of the brain, thus contributing to POD. PE (40:7e) might

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Section: Discussionmentioning

confidence: 99%

Metabolomic and Lipidomic Profiling of Preoperative CSF in Elderly Hip Fracture Patients With Postoperative Delirium

Han

Zhang

Liu

et al. 2020

Front. Aging Neurosci.

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“…Nevertheless, it has been shown that hyperoxia preconditioning significantly decreased the brain LPC levels and ischemic brain injury (27), suggesting an important association of LPC content with brain injury. Excessive conversion of PC to LPC appears to be detrimental to the brain recovering from cerebral ischemia.…”

Section: Introductionmentioning

confidence: 99%

An imbalanced ratio between PC(16:0/16:0) and LPC(16:0) revealed by lipidomics supports the role of the Lands cycle in ischemic brain injury

Zheng

Xie

Zheng

et al. 2021

Journal of Biological Chemistry

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Promoting brain recovery after stroke is challenging as a plethora of inhibitory molecules are produced in the brain preventing it from full healing. Moreover, the full scope of inhibitory molecules produced is not well understood. Here, using a high-sensitivity UPLC-MS-based shotgun lipidomics strategy, we semiquantitively measured the differential lipid contents in the mouse cerebral cortex recovering from a transient middle cerebral artery occlusion (MCAO). The lipidomic data were interrogated using the soft independent modeling of class analogy (SIMCA) method involving principal component analysis (PCA) and orthogonal partial least squares discriminant analysis (OPLS-DA). Statistics of the 578 confirmed lipids revealed 84 species were differentially changed during MCAO/reperfusion. The most dynamic changes in lipids occurred between 1 and 7 days post-MCAO, whereas concentrations had subsided to the Sham group level at 14 and 28 days post-MCAO. Quantitative analyses revealed a strong monotonic relationship between the reduction in phosphatidylcholine (PC)(16:0/16:0) and the increase in lysophosphatidylcholine (LPC)(16:0) levels (Spearman’s Rs = −0.86) during the 1 to 7 days reperfusion period. Inhibition of cPLA2 prevented changes in the ratio between PC(16:0/16:0) and LPC(16:0), indicating altered Land’s cycle of PC. A series of in vitro studies showed that LPC(16:0), but not PC(16:0/16:0), was detrimental to the integrity of neuronal growth cones and neuronal viability through evoking intracellular calcium influx. In contrast, PC(16:0/16:0) significantly suppressed microglial secretion of IL-1β and TNF-α, limiting neuroinflammation pathways. Together, these data support the role of the imbalanced ratio between PC(16:0/16:0) and LPC(16:0), maintained by Lands’ cycle, in neuronal damage and microglia-mediated inflammatory response during ischemic recovery.

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“…On the other hand, the Rf value is not sufficient for the detection of compounds on the TLC plate; as a result, each spot was picked up from the plate and the predicted targets of compounds were investigated using offline mass spectrometry. The molecular weight of various lipids in the rat brain samples is shown in our previous study (19).…”

Section: Esi/it Mass Spectrometrymentioning

confidence: 80%

Prolonged and Intermittent Bilateral Common Carotid Artery Occlusion Induces Brain Lipidome Changes in a Rat Stroke Model

Faezi

Bigdeli

2016

Thrita

Self Cite

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Background: Recent studies suggest that prolonged and intermittent bilateral common carotid artery occlusion (prolonged bilateral common carotid artery occlusion (PO) and intermittent bilateral common carotid artery occlusion, respectively) can lead to reduced ischemia brain injury in ischemic tolerance. Objectives: In this study, we aimed to investigate the changes in brain lipidomics following prolonged and intermittent ischemic preconditioning. Materials and Methods: Two groups underwent bilateral common carotid artery occlusion either intermittently (for 3 continuous periods within a timeframe of 20 minutes, releasing 3 consecutive times, yielding a total of 9 minutes (intermittent bilateral common carotid artery occlusion)) or for 9 minutes continuously (prolonged bilateral common carotid artery occlusion). The third and fourth groups were used as control and sham (without ischemia) groups, respectively. The first three groups were subdivided into middle cerebral artery occlusion-operated (middle cerebral artery occlusion MCAO), for 60 minutes of ischemia) and intact (without any surgery) subgroups. After 1 hour of ischemia and 24 hours of reperfusion, the neurologic deficit score (neurological deficit score (NDS)) and the infarct volume (infarct volume) were assessed in the middle cerebral artery occlusion-operated subgroup. Brain lipidomics were measured in the intact subgroup and the sham group. Results: Preconditioning with prolonged bilateral common carotid artery occlusion and intermittent bilateral common carotid artery occlusion significantly decreased the neurological deficit scores and infarct volume and increased the levels of phosphatidylethanolamine, sphingomyelin, cholesterol ester, cholesterol, phosphatidylcholine, and cerebroside in the brain compared with the control and sham groups. Prolonged bilateral common carotid artery occlusion and intermittent bilateral common carotid artery occlusion significantly decreased the brain ceramide and lysophosphatidylcholine levels. The triglyceride levels in both groups (intermittent bilateral common carotid artery occlusion and prolonged bilateral common carotid artery occlusion) did not change in comparison with the control and sham groups. Conclusions: Although it seems that further studies are needed to clarify the real mechanisms of ischemic tolerance, ischemic preconditioning could decrease brain ischemia injury via changes in brain lipidomics.

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Normobaric Hyperoxia Preconditioning Induces Changes in the Brain Lipidome

Cited by 4 publications

References 0 publications

Metabolomic and Lipidomic Profiling of Preoperative CSF in Elderly Hip Fracture Patients With Postoperative Delirium

Metabolomic and Lipidomic Profiling of Preoperative CSF in Elderly Hip Fracture Patients With Postoperative Delirium

An imbalanced ratio between PC(16:0/16:0) and LPC(16:0) revealed by lipidomics supports the role of the Lands cycle in ischemic brain injury

Prolonged and Intermittent Bilateral Common Carotid Artery Occlusion Induces Brain Lipidome Changes in a Rat Stroke Model

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