β-Asarone Inhibits Neuronal Apoptosis via the CaMKII/CREB/Bcl-2 Signaling Pathway in an in vitro Model and AβPP/PS1 Mice

Objective Common inhalation anesthetics used for clinical anesthesia (such as sevoflurane) may induce nerve cell apoptosis during central nervous system development. Furthermore, anesthetics can produce cognitive impairments, such as learning and memory impairments, that continue into adulthood. However, the precise mechanism remains largely undefined. We aimed to determine the function of microRNA-1297 (miR-1297) in sevoflurane-induced neurotoxicity. Methods Reverse transcription-polymerase chain reaction assays were used to analyze miR-1297 expression in sevoflurane-exposed mice. MTT and lactate dehydrogenase (LDH) assays were used to measure cell growth, and neuronal apoptosis was analyzed using flow cytometry. Western blot analyses were used to measure PTEN, PI3K, Akt, and GSK3β protein expression. Results In sevoflurane-exposed mice, miR-1297 expression was up-regulated compared with the control group. MiR-1297 up-regulation led to neuronal apoptosis, inhibition of cell proliferation, and increased LDH activity in the in vitro model of sevoflurane exposure. MiR-1297 up-regulation also suppressed the Akt/GSK3β signaling pathway and induced PTEN protein expression in the in vitro model. PTEN inhibition (VO-Ohpic trihydrate) reduced PTEN protein expression and decreased the effects of miR-1297 down-regulation on neuronal apoptosis in the in vitro model. Conclusion Collectively, the results indicated that miR-1297 stimulates sevoflurane-induced neurotoxicity via the Akt/GSK3β signaling pathway by regulating PTEN expression.

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Neuronal Apoptosis in an in Vitro Model of Photochemically Induced Oxidative Stress

Experimental Neurology ◽

10.1006/exnr.1995.1022 ◽

1995 ◽

Vol 133 (2) ◽

pp. 198-206 ◽

Cited By ~ 27

Author(s):

Hari Manev ◽

Cinzia M. Cagnoli ◽

Cagla Atabay ◽

Elena Kharlamov ◽

Miloš D. Ikonomović ◽

...

Keyword(s):

Oxidative Stress ◽

Neuronal Apoptosis ◽

In Vitro Model ◽

Vitro Model

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Transcriptomic Analysis Implicates the p53 Signaling Pathway in the Establishment of HIV-1 Latency in Central Memory CD4 T Cells in an In Vitro Model

PLoS Pathogens ◽

10.1371/journal.ppat.1006026 ◽

2016 ◽

Vol 12 (11) ◽

pp. e1006026 ◽

Cited By ~ 14

Author(s):

Cory H. White ◽

Bastiaan Moesker ◽

Nadejda Beliakova-Bethell ◽

Laura J. Martins ◽

Celsa A. Spina ◽

...

Keyword(s):

T Cells ◽

Signaling Pathway ◽

Cd4 T Cells ◽

In Vitro Model ◽

P53 Signaling ◽

Vitro Model ◽

Memory Cd4 T Cells ◽

P53 Signaling Pathway ◽

Hiv 1

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Gal-3 is a potential biomarker for spinal cord injury and Gal-3 deficiency attenuates neuroinflammation through ROS/TXNIP/NLRP3 signaling pathway

Bioscience Reports ◽

10.1042/bsr20192368 ◽

2019 ◽

Vol 39 (12) ◽

Cited By ~ 6

Author(s):

Zhouliang Ren ◽

Weidong Liang ◽

Jun Sheng ◽

Chuanhui Xun ◽

Tao Xu ◽

...

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Signaling Pathway ◽

In Vitro Model ◽

Sd Rat ◽

Potential Biomarker ◽

Cord Injury ◽

Vitro Model

Abstract Spinal cord injury (SCI) often occurs in young and middle-aged population. The present study aimed to clarify the function of Galectin-3 (Gal-3) in neuroinflammation of SCI. Sprague–Dawley (SD) rat models with SCI were established in vivo. PC12 cell model in vitro was induced by lipopolysaccharide (LPS). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Gene chip were used to analyze the expression levels of genes in the signaling pathway. Histological assessment, ELISA and Western blotting were conducted to evaluate the effects of Gal-3 upon the SCI model. In the in vivo SD rat model, Gal-3 expression level was up-regulated. The inhibition of Gal-3 attenuated the neuroinflammation in SCI model. The inhibition of Gal-3 could also mitigate the neuroinflammation and reactive oxygen species (ROS) in in vitro model. ROS reduced the effect of Gal-3 on oxidative stress in in vitro model. Down-regulating the content of TXNIP decreased the effect of Gal-3 on neuroinflammation in in vitro model. Suppressing the level of NLRP3 could weaken the effect of Gal-3 on neuroinflammation in in vitro model. Our data highlight that the Gal-3 plays a vital role in regulating the severity of neuroinflammation of SCI by enhancing the activation of ROS/TXNIP/NLRP3 signaling pathway. In addition, inflammasome/IL-1β production probably acts as the therapeutic target in SCI.

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