Postoperative cognitive dysfunction (POCD) is a common surgical complication that causes additional pain in patients and affects their quality of life. To address this problem, emerging studies have focused on the POCD. Recent studies have shown that aging and anesthetic exposure are the two major risk factors for developing POCD. However, few reports described the exact molecular mechanisms underlying POCD in elderly patients. In the previous studies, the endoplasmic reticulum (ER) stress and neuroapoptosis in the hippocampus were associated with inducing POCD; however, no further information on the related signaling pathways could be disclosed. The PERK-eIF2α-ATF4-CHOP pathway is identified as the main regulatory pathway involved in ER stress and cell apoptosis. Therefore, we assume that the occurrence of POCD induced by sevoflurane inhalation may potentially result from ER stress and neuroapoptosis in the hippocampus of aged mice mediated by the PERK-eIF2α-ATF4-CHOP pathway. In our study, we found a relationship between sevoflurane inhalation concentration and memory decline in aged mice, with a ‘ceiling effect’. We have confirmed that POCD induced by sevoflurane results from ER stress and neuroapoptosis in the hippocampus of aged mice, which is regulated by the over-expression of PERK-eIF2α-ATF4-CHOP pathway. Furthermore, we also showed that the dephosphorylation inhibitor of eIF2α (salubrinal) could down-regulate PERK-eIF2α-ATF4-CHOP pathway expression to inhibit ER stress and enhance the cognitive function of aged mice. In general, our study has elucidated one of the molecular mechanisms of sevoflurane-related cognitive dysfunction in aged groups and provided new strategies for treating sevoflurane-induced POCD. 

The role of PERK-eIF2α-ATF4-CHOP pathway in sevoflurane induced neuroapoptosis and cognitive dysfunction in aged mice.

Traumatic brain injury (TBI) is an important cause of disability and death. TBI leads to multiple forms of nerve cell death including ferroptosis due to iron-dependent lipid peroxidation. Anacardic acid (AA) is a natural component extracted from cashew nut shells, which has been reported to have neuroprotective effects in traumatic brain injury. We investigated whether AA has an anti-ferroptosis effect in TBI.We used the Feeney free-fall impact method to construct a TBI model to investigate the effect of AA on ferroptosis caused by TBI, in which Ferrostatin-1 (Fer-1), a ferroptosis inhibitor, served as a positive control group. We first identified the therapeutic effect of AA on TBI through modified neurological severity score (mNSS) and determined the appropriate concentration. Secondly, we investigated the effect of AA on the expression level of the key protein of ferroptosis by Western blotting and immunohistochemistry. Then the effect of AA on nerve tissue injury and nerve function improvement was verified. Finally, enzym-linked immunosorbent assay (ELISA) was used to verify that AA could reduce inflammation after TBI.We found the intensely inhibitory effect of AA on ferroptosis, which is in parallel with the results obtained after Fer-1 treatment. In addition, AA and Fer-1 mitigated TBI-mediated tissue defects, destruction of the blood-brain barrier, and neurodegeneration. Novel object recognition (NOR), mNSS and water maze test showed that AA could significantly reduce the impairment of neural function and behavioral cognitive ability caused by TBI. Finally, we also demonstrated that AA has not only an anti-ferroptosis effect, but also an anti-inflammation effect.AA can reduce the neurological impairment and behavioral cognitive impairment caused by TBI through the dual effect of anti-ferroptosis and anti-inflammation. 

Anacardic acid improves neurological deficits in traumatic brain injury by anti-ferroptosis and anti-inflammation

Traumatic brain injury (TBI) can disrupt the blood–brain barrier and cause loss of neuronal functions. The neuroprotective effects of exogenous basic fibroblast growth factor (FGF2) have been demonstrated. However, these effects diminish with decreasing FGF2 activity. To address this issue, in this study, a multifunctional system with high affinity for growth factors (GelMA-HDC) was developed to deliver growth factors to the brain and provide protection and regeneration in cases of TBI. The results revealed that GelMA-HDC, an injectable hydrogel consisting of gelatin-methacryloyl (GelMA) and heparin-dopamine conjugate (HDC), had a smaller pore size, higher adhesiveness, and softer mechanical properties than the GelMA hydrogel. Moreover, GelMA-HDC increased the stability of FGF2 and enabled controlled FGF2 release in brain lesions. The FGF2-HDC complex exhibited a robust neuroprotective effect by augmenting the FGF2-FGFR1 signaling pathway. Furthermore, the implantation of GelMA-HDC hydrogels at the lesion site in TBI mice exhibited significant reparative potential, encompassing the regeneration of impaired cortical tissues, suppression of neuroinflammation, promotion of neuronal survival, and rescue of learning and memory functions in mice. Therefore, this study presents initial findings on the use of mussel-inspired GelMA-based hydrogels with high affinity for FGFs to treat TBI. This innovative approach holds significant potential for the clinical use of heparin-binding FGFs for repairing TBI or other neurological diseases. 

Ultrasoft bioadhesive hydrogel as a versatile platform for the delivery of basic fibroblast growth factor to repair traumatic brain injury

Traumatic brain injury (TBI) affects millions of people each year and in many cases results in long term disabilities. Once a TBI has occurred, there is significant breakdown of the blood-brain barrier resulting in increased vascular permeability and progression of the injury. In this study we investigated the use of an infusible extracellular matrix derived biomaterial (iECM) for its ability to reduce vascular permeability and modulate gene expression in the injured brain. First, we characterize the pharmacokinetics of iECM administration in a mouse model of TBI and demonstrate robust accumulation of iECM at the site of injury. Next, we show that iECM administration after injury can reduce the extravasation of molecules into the brain, and in vitro, iECM increases trans-endothelial electrical resistance (TEER) across a monolayer of TNFα-stimulated endothelial cells. In gene expression analysis of brain tissue, iECM induces changes that are indicative of downregulation of the pro-inflammatory response 1 day post-injury/treatment and neuroprotection at 5 days post-injury/treatment. Therefore, iECM shows potential as a treatment for TBI. This article is protected by copyright. All rights reserved.

https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/adhm.202300782

Infusible Extracellular Matrix Biomaterial Promotes Vascular Integrity and Modulates the Inflammatory Response in Acute Traumatic Brain Injury.

Salinity, an important abiotic stress, affects arable land worldwide, reducing crop growth, yield and quality. Lettuce ( Lactuca sativa L .), which is very sensitive to salt stress, is one of the crops affected by soil salinity and salt (NaCl) stress also affects lettuce cultivation. Different plant growth regulators (salicylic acid (SA), polyamines, glycine betaine (GB) and melatonin (MEL)) are used to reduce the harmful effects of soil salinity. In this study, the effects of NaCl and MEL treatments on physiological parameters (cell membrane damage (%), leaf relative water content (RWC%), chlorophyll amount), DNA methylation and some NaCl tolerance genes ( SOS1 , SOS2 , AKT1 , NHX1 , HKT1 ) have examined in two different lettuce genotypes (Yedikule and Ivanka). When the effect of NaCl stress on physiological parameters was examined, it was detected that this stress increased cell membrane damage and decreased chlorophyll content and RWC %. The effects of MEL applications together with NaCl stress on these parameters were positive. In the gene expression analysis results, it was determined that SOS1 , SOS2 , AKT1 , NHX1 and HKT1 gene expressions increased in both lettuce genotypes and decreased in MEL applications. On the flip side, according to methylation sensitive amplification polymorphism (MSAP) findings, while a decrease in methylation level was determined in NaCl stress compared to the control in both genotypes. Methylation levels increased compared to NaCl stress in MEL applications with NaCl stress, but this rate was still lower than the control. According to the results obtained, it was concluded that exogenous MEL application in lettuce genotypes is important in response to NaCl stress. 

/pdf/the-effect-of-melatonin-on-some-physiological-parameters-2e8gkp9m.pdf

THE EFFECT OF MELATONIN ON SOME PHYSIOLOGICAL PARAMETERS, SALT SENSOR GENES AND DNA METHYLATION IN SALT STRESSED LETTUCE ( Lactuca Sativa L.)

Traumatic brain injury (TBI) is a kind of acquired brain injury, which is caused by external mechanical forces. Moreover, the neuroprotective role of sevoflurane (Sevo) has been identified in TBI. Therefore, this research was conducted to figure out the mechanism of Sevo in TBI via FGF2.The key factors of neuroprotective effects of Sevo in TBI rats were predicted by bioinformatics analysis. A TBI model was induced on rats that then inhaled Sevo for 1 h and grouped via lentivirus injection. Modified Neurological Severity Score was adopted to evaluate neuronal damage in rats, followed by motor function and brain water content measurement. FGF2, EZH2, and HES1 expression in brain tissues was evaluated by immunofluorescence staining, and expression of related genes and autophagy factors by RT-qPCR and Western blot analysis. Methylation-specific PCR was performed to assess HES1 promoter methylation level, and ChIP assay to detect the enrichment of EZH2 in the HES1 promoter. Neuronal damage was assessed by cell immunofluorescence staining, and neuronal apoptosis by Nissl staining, TUNEL staining, and flow cytometry.Sevo diminished brain edema, improved neurological scores, and decreased neuronal apoptosis and autophagy in TBI rats. Sevo preconditioning could upregulate FGF2 that elevated EZH2 expression, and EZH2 bound to the HES1 promoter to downregulate HES1 in TBI rats. Also, FGF2 or EZH2 overexpression or HES silencing decreased brain edema, neurological deficits, and neuronal autophagy and apoptosis in Sevo-treated TBI rats.Our results provided a novel insight to the neuroprotective mechanism of Sevo in TBI rats by downregulating HES1 via FGF2/EZH2 axis activation. 

/pdf/the-neuroprotective-mechanism-of-sevoflurane-in-rats-with-270dj0u0.pdf

The neuroprotective mechanism of sevoflurane in rats with traumatic brain injury via FGF2

Physiological response of barley seedlings to salinity and artemisinin combined stresses under freeze-thaw environment

https://jneuroinflammation.biomedcentral.com/track/pdf/10.1186/s12974-021-02348-z

The dynamic interferometry is used to overcome the problem of the vibration and the air turbulence present in the testing
process of concave aspherical mirror, whose aperture is extra large, and optical path is extra long. Aiming to 4.5m
aperture concave mirror, two schemes have been designed: offner refractive and reflective compensators. The analytical
model of the theoretical error analysis under the dynamic interferometry condition has been built. According to the result
we can come to a conclusion that using the method of dynamic interferometry, the accuracy of measuring can be reached
within λ/80. The optical testing path of mirror with multiple segments has been designed in the end. Results of this paper
could provide references for the design, processing, assembling and testing technologies of large or extra large optical
system.

The dynamic interferometry technology of 4.5-meter concave aspherical mirror and relativity precision analysis

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The neuroprotective mechanism of sevoflurane in rats with traumatic brain injury via FGF2

Physiological response of barley seedlings to salinity and artemisinin combined stresses under freeze-thaw environment

The neuroprotective mechanism of sevoflurane in rats with traumatic brain injury via FGF2

The dynamic interferometry technology of 4.5-meter concave aspherical mirror and relativity precision analysis