Transient changes in blood‐brain barrier integrity, thermotolerance, and heat shock protein expression following brief hyperthermia in an in vitro model

This study aimed to investigate the antistress properties of the ethanol extract ofCymbopogon schoenanthus(CSEE), growing wild in the southern part of Tunisia. The effect of extracts on H2O2-induced cytotoxicity and stress in human neuroblastoma SH-SY5Y cells. Its effect on stress-induced in ICR mice was exposed to force swim and tail suspension, in concordance with heat shock protein expression (HSP27 and HSP90), corticosterone, and catecholamine neurotransmitters level. Our results demonstrated that pretreatment of SH-SY5Y cells with CSEE at 1/2000, 1/1000, and 1/500 v/v dilutions significantly inversed H2O2-induced neurotoxicity. Moreover, CSEE treatments significantly reversed heat shock protein expression in heat-stressed HSP47-transformed cells (42°C, for 90 min) and mRNA expression of HSP27 and HSP90 in H2O2-treated SH-SY5Y. Daily oral administration of 100 mg/kg and 200 mg/kg CSEE was conducted to ICR mice for 2 weeks. It was resulted in a significant decrease of immobility time in forced swimming and tail suspension tests. The effect of CSEE on animal behavior was concordant with a significant regulation of blood serum corticosterone and cerebral cortex levels of catecholamine (dopamine, adrenaline, and noradrenaline). Therefore, this study was attempted to demonstrate the preventive potential of CSEE against stress disorders atin vitroandin vivolevels.

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The isolated neonatal rat-cardiomyocyte used in an in vitro model for ‘ischemia’. II. Induction of the 68 kDa heat shock protein

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research ◽

10.1016/0167-4889(91)90190-9 ◽

1991 ◽

Vol 1091 (3) ◽

pp. 278-284 ◽

Cited By ~ 22

Author(s):

Mark J.M. Tuijl ◽

Paul M.P. van Bergen en Henegouwen ◽

Roeland van Wijk ◽

Arie J. Verkleij

Keyword(s):

Heat Shock ◽

Heat Shock Protein ◽

In Vitro Model ◽

Neonatal Rat ◽

Vitro Model

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MicroRNA-1297 suppressed the Akt/GSK3β signaling pathway and stimulated neural apoptosis in an in vivo sevoflurane exposure model

Journal of International Medical Research ◽

10.1177/0300060520982104 ◽

2021 ◽

Vol 49 (4) ◽

pp. 030006052098210

Author(s):

Quan Wang ◽

Jingcong Luo ◽

Ruiqiang Sun ◽

Jia Liu

Keyword(s):

Protein Expression ◽

Signaling Pathway ◽

Neuronal Apoptosis ◽

In Vitro Model ◽

Nervous System Development ◽

Exposure Model ◽

Control Group ◽

Pten Protein ◽

Vitro Model

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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